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Interstitial Gingivitis 


EUGENE hi. TALBOT, M. D., D. D. S. 

Pkofessok of Dental and Dual surgery, Northwestern I'nivf.rsity. Woman's .Medical 
Honorary President of the Dental Section of the Tenth International Medical Congress, 
Berlin, 1890; Honorary President of the Dental Section of the Twelfth International 
Medical Congress, Moscow, 1897; Honorary Secretary of the Pan-American Medical 
Congress. Washington. 1893; Member of the American Medical Association; Fellow 
of the Chicago Academy of Medicine; Member of the Chicago Medical Society; 
Secretary of the Section on Stomatology of the American Medical Asso- 
ciation; Member of the Chicago Academy of Sciences; Honorary Member 
of the odontologischen gesellschaft, berlin, germany; membre 
Honoraire de l' Association Generale des Dentistes de France; 
Honorary Member Sociedad Odontologia Kspanola; Author of 
"The Irregularities of the Teeth and their Treatment" 
Author of " Chart of Typical Forms of Constitutional 
Irregularities of the Teeth"; Author of "The Eti- 
ology of Osseous Deformities of the Head, Face, 
Jaws and Teeth". Author of "Degeneracy, its 
Causes. Signs and Results"; Kic. I'm- 

with seventy-three illustrations. 



1 899. 

Entered According to Act of Congress, in the Year 1899, by 

Eugene S. Talbot, 
the Office of the Librarian of Congress at Washington, D. C. 


This Work, 

As a Slight Token of Appreciation of Their Contributions to Science, 

is Respectfully Dedicated. 

Digitized by the Internet Archive 

in 2012 with funding from 

LYRASIS Members and Sloan Foundation 


The great law of medical science, that to know the cause is 
half the treatment, is as applicable to dentistry as to any other 
specialty of medicine, and is as applicable to dental problems as 
to those of biology generally. Treatment of any disease without 
knowledge of its pathology is practically a failure. 

While much has been written upon the pyorrhceic stage of 
interstitial gingivitis and its treatment, during the past two 
decades, no new principle has been advanced whereby the parts 
can be restored to a healthy condition, or whereby the disease 
can he prevented. The disease is admittedly on the increase. 
This seems at first sight to indicate that dental prophylaxis and 
treatment, so tar as this disease is concerned, is a failure. 

Other specialists restore patients to health. Nearly every 
patient with this disease applies to dentists. Most dentists, how- 
ever, hardly know the disease exi.--.ts and much less arc capable 
of ottering suggestions as to treatment. It seems strange that in 
America so little original work has been done upon a disease 
more to be dreaded than tooth decay. Treatment has been 
wholly at random, and hence, as a rule, only to limited extent 
successful. Destruction of the alveolar process and loss of the 
teeth is so rapidly sure that the necessity for dental scientists to 
solve the etiology of this very common disease seems imperative. 

Nearly two decades ago I felt and expressed the necessity for 
more extended study (Dental Cosmos, 188(5, page C>S ( .)) of the 
clinical aspects and etiology of this disease. Even during appar- 
ently diverse and separated studies, such as those related to dental 
and maxillary irregularities and degeneracy, the necessity for 
this has forced itself still further upon me. In the present 
study, the disease has, of necessity, been considered from the 
broad standpoint of general pathology. In all instances where 
possible personal elements of error are present, these have been 
eliminated bv having researches made bv more than one observer. 

The attempt has been made to summarize all researches on 
the subject. So much have opinions been intermingled that it is 
possible that proper credit for priority has unintentionally not 
been given. 

The author is under obligation to the following scientists for 
their kind assistance : Dr. Ludwig Hektoen, Pathologist, Rush 
Medical College ; Dr. Jerome H. Salisbury, Chemist, Rush 
Medical College ; Dr. W. A. Evans, Pathologist, Columbus Med- 
ical Laboratory, Professor of Pathology, Chicago College of 
Physicians and Surgeons and Milwaukee Medical College ; Dr. 
J. A. Wesener. Chemist, Columbus Medical Laboratory, Profes- 
sor of Chemistry, Chicago College of Physicians and Surgeons ; 
Dr. Vida A. Latham, Pathologist, Northwestern University, 
Woman's Medical School; Dr. Maximilian Herzog, Pathologist, 
Chicago Polyclinic Hospital ; Professor Theo. A. Edwin Klebs 
and Dr. Robert F. Zeit, Pathologists, and Dr. W. L. Baum, 
Professor of Diseases of the Skin, Post-Graduate Medical School, 
Chicago ; Dr. G. V. I. Brown, Professor of Oral Surgery, Dental 
Department, Milwaukee Medical College; Dr. Frederick Noyes, 
Histologist, Dental Department, Northwestern University ; Dr. 
J. G. Kiernan, and to Blomgren Bros. & Co. for electrotypes, etc. 

103 State Street, Chicago. 



I. History . . . . . . . .1 

II. Introduction ........ 10 

III. Transitory Structures — 

The Jaws * . .2(1 

The Alveolar Process ..... 21 

Periosteum and Peridental Membrane . 33 

The Gums -and Mucous Membrane ... 42 

Do Glands Exist in Epithelial and Peridental Mem- 
brane? ........ 47 

Bone Building and Absorption .... 59 

IV. Theories of Interstitial Gingivitis . . . .65 
V. Uric Acid and Interstitial Gingivitis ... 68 

VI. Inorganic Salts and Interstitial Gingivitis . . 73 

VII. Heredity and Environment ..... 83 

VIII. Degeneracy and Degenerate Tissues . . . .86 

IX. Neurotic, Diathetic and Degenerate Children . . 89 

X. Interstitial Gingivitis in Dogs . . . . .98 

• XI. -Mercurial Interstitial Gingivitis in Dons . 117 

XII. Bacteriology of Interstitial Gingivitis . . . 122 

XIIL Scorbutic Interstitial Gingivitis in Man . . . 127 

XIV. Interstitial Gingivitis in Man from Metallic and Other 

Drug Action . . . . . . .142 

XV. Conclusions . . . . . . . .146 

Pathogenesis of Interstitial Gingivitis . . 151 

Endarteritis Obliterans ..... 154 

Absorption of the Alveolar Process . . . 157 

Pyorrhcka Alveoi.aris from Interstitial Gingivitis . 162 
Constitutional Effects of Pyorrhcea Alveolaris . 167 
Calcic Deposits ....... 168 

XVI. Treatment . . . ... . .172 





Inflammation of the peridental membrane is probably coeval 
with man. Some of the skulls found earliest in the cave-dwell- 
ing period exhibit evidences of its presence. In some of these, 
careful observation lias shown deposits encroaching upon the 
roots of the teeth and resultant absorption of the alveolar 

In the Swiss lake-dwellings and in the earlier Irish cran- 
noges of like construction and situation, skulls are found, which 
exhibit deposits of tartar, inflammation of the peridental mem- 
brane and al (sorption of the alveolar process. These skulls were 
those of primitive races in whom disease of the jaws and teeth i- 
supposed to he absent or infrequent. In the skulls of the peo- 
ples exhibiting the highest civilization at the earliest period — 
those of the Accadians and Egyptians — similar inflammatory 
conditions are to be found. This, however, was to have been 
expected, to judge from the dental directions left among the 
medical records of these peojjies. The Greeks, Syrians, Arab- 
ians, Dravidians and Aryans of India and the early Burmese 
all suffered from this disorder. In the museum at Constan- 
tinople are the skulls of soldiers who fought at a battle 328 
B. C. One of these skulls has the anterior alveolar process 
entirely absorbed away. The roots of the right central, the 
right lateral and the left central incisors are exposed. 

Inflammation of the peridental membranes, it will be evident, 
is, therefore, not a modern disease; not a disease confined either 
to civilized or primitive races, hut one which attacked man early 


in his evolution. Like most diseases it has been chiefly dis- 
cussed and analyzed during the past two centuries. 

In 1740 H. A. Fauchard ' (while recognizing the disease in 
all its essential features and describing its principal symptoms) 
advanced no theory as to its origin. 

In 1778 M. Jourdain 2 advanced the opinion that the disease 
was of scorbutic origin. 

In 1821 L. Kaecker 3 discussed the disorder in an essay on 
the devastations of the gums and alveolar processes. 

In 1822 M. Joirac 4 (in a discussion of the disease), Avhile 
advancing no theory as to its origin, called it " pyorrhoea inter- 
al veolo-dentai re. ' ' 

In 1860 Marshall de Calve 5 advanced the opinion that the 
disorder was of hereditary origin. 

In 1867 Magitot, discussing the disorder, advanced the 
opinion that the gum, being in all cases only attacked subse- 
quently, is not the original seat of the lesion. In his opinion 
systemic disorders like gout, rheumatism, albuminuria, diabetes 
and anaemia had an influence. 

Bonwill 6 during the same year expressed the opinion that 
the disorder was due to thinness of the alveolar process between 
the teeth, thus depriving the peridental membrane and gum 
tissue of proper support, The want of proper articulation of 
the teeth also exerted an influence. 

In 1870 Brown ascribed the disorder to seminal calculus. 

In 1875 John T. Riggs, after whom the disorder is frequently 
called, entitled it (in a paper read before the American 
Academy of Dental Surgery) suppurative inflammation of the 
gums and absorption of the gums and alveolar process. 

During the same year Scheff 7 of Vienna entitled the disorder 
periostitis dentalis. He was of the opinion that it originated 
from external irritation through mechanical, thermic and chemic 
changes. The real origin of the disorder was, in his opinion, 

1 Independent Dental Journal, 1875. 

2 Philadelphia Journal of Medical and Physical Science, 1821. 

3 International Dental Journal, Vol. XIII. 

4 Journal of the American Medical Association. 

5 Journal of the American Medical Association. 
G Dental Cosmos, Vol. XXIV. 

7 Wiener Med. Presse, Vol. XVI. 

very often obscure. He doubted, however, the influence of 

In 1876 Sirlctti ' ( in a discussion of the pathology of the 
disorder, which he called alveolo-dental periostitis) regarded it as 
due to constitutional conditions, like rheumatism, scrofula, syph- 
ilis, etc., with local causes as exciting factors. 

In 1S77 Rehwinkle, 2 in a paper on pyorrhoea alveolaris, after 
citing from Albright (of Berlin) the claim that the disorder 
was due to unclean liness, mercury and the suppression of habitual 
secretions, expressed the opinion that acquired and inherited 
constitutional defect often played an important part as etiologic 
factors. He was also of opinion that mercury exerted an influ- 
ence in its causation. Salivary deposits were, in his opinion, 
without influence. Clowes 3 was of opinion in 1879 that the 
general cause was lack of nutrition in the parts. The use of 
wedges often excited the disorder. 

C. J. Essig, 4 in 1880, expressed the opinion that its predis- 
posing causes were unknown, that it occurred as a rule in healthy 
persons, and that irregular and crowded teeth acted as an exciting 

In another paper during the same year G. A. Mills 5 expressed 
the opinion that the disorder was of systemic origin. Various 
mental and physical influences aided its progress, such as nervous 
exhaustion and bodily and mental overwork. In his opinion it 
frequently occurred in children and adolescents from eruptive 
fevers. The deposit was only a local manifestation of the 

In 1881 X. S. Niles 6 expressed the opinion that constitutional 
conditions were, as a rule, without influence, and that local irrita- 
ting deposits were the cause in twenty-five per cent of the cases 
coming under his observation. He was of opinion also that the 
amount of lime salts taken into the system in drinking water 
exerted an influence. A calcic and phosphatic diathesis had an 
influence in the production of the disorder. 

■Gazzetta Medica di Roma, ls7(i. 
-Dental Cosmos, Vol. XIX. 
'Ibid., Vol. XXI. 

4 Dental Cosmos, Vol. X XI. 

5 Ibid., Vol. XXIII. 

6 Ibid., Vol. XXIV. 


In 1881 (when there seemed to have been many contributions 
to the literature of the subject) Atkinson 1 expressed the opinion 
that nervous debility or original defect in innervation exerted an 
influence in the production of the disorder. The deposits of 
tartar were a secondary consequence. In the course of his paper 
he cited the opinion of Hamilton Cartwright that Riggs's disease 
commenced in an unhealthy condition of the gums with a sec- 
ondary deposit of tartar. 

In a paper read before the Dental Section of the Inter- 
national Medical Congress, Walker 2 claimed that the starting 
point of the disease was subacute inflammation passing into the 
depths of the alveolar process adjacent to the inflamed gum. In 
the discussion of this paper, Archovy and Joseph Izklai, of 
Buda Pesth, ascribed the disorder to minute organisms. Oakley 
Coles thought that systemic states were the predisposing factors, 
while minute organisms exerted an exciting influence. 

In 1882, L. C. Ingersol 3 regarded sanguinary calculus as a 
manifestation of the disorder, and distinguished it from salivary 

Malasses and Gallippe, 4 in 1884, expressed the opinion that 
the disorder was of microbic origin. 

In 1885, A. O. Rawls 5 expressed the opinion that the causes 
were environment with morbid factors, such as malaria, excessive 
sodium, etc., chloride and mercury. 

In 1886, Reese 6 expressed the opinion that the disorder had 
its source in the uric acid diathesis resultant on abuse of 

During the same year, J. D. Patterson 7 expressed the opinion 
that the disorder was of catarrhal origin. Later, in 1886, J. N. 
Farrar 8 regarded the disorder as a combined result of systemic 
tendencies and local irritants. There was a peculiar condition of 
the system associated with hypersecretion laden with increased 
earthy deposits. 

1 Dental Cosmos, Vol. XXIV. 

2 Transactions of the International Medical Congress, 1881. 

3 Dental Cosmos, Vol. XXV. 

4 Ibid., Vol. XXVI. 

5 Ibid., Vol. XXVII. 

fi Independent Practitioner, Vol. VI. 

7 Dental Cosmos, Vol. XXI. 

8 Independent Practitioner, Vol. VII. 

A. R. Starr later also expressed the same opinion. He, how- 
ever, was unable to determine the local irritation factor, but 
regarded it as the same as that which causes exostosis of the 
cementum. He had found most cases in the upper jaws. 

Black 1 designated the disorder phagadenic pericementitis. It 
was a specific infection of an inflammatory character, having its 
origin in the gingiva, and was accompanied with destruction of 
the peridental membrane and alveolar walls. 

E. S. Talbot J during the same year regarded the disorder as 
a local one, due to both local and constitutional causes. The 
disorder began with simple inflammation of the gums, which 
afterward became chronic. 

Of the status of this disease at the close of the year 1887, 
the following analytic picture was drawn by W. X. Sudduth 3 : 
Pyorrhoea alveolaris is a term applied to the secondary stage- of 
a disease that has its inception in a catarrhal stomatitis. Being 
confined, as a rule, to the margin of the gums surrounding the 
teeth, it might be called a " gingivitis," w T ere it not for the gen- 
eral catarrhal tendency shown by the entire mucous membrane 
of the mouth and nasal passages. The intimate relation between 
a general catarrhal idiosyncrasy and pyorrhoea alveolaris is more 
than mere coincidence. Its common occurrence in persons who 
have irregular teeth has also been often noted by Dr. Sudduth. 
who considers that this fact has, besides the matter of uncleanli- 
ne>s, a direct bearing upon its pathogeny. It is well known that 
the irregularities of the teeth present an indication of a degener- 
ative taint, and that persons in whom irregularities occur are 
very prone to catarrhal affections of the respiratory organs, 
including the nasal passage. Their skin is usually very suscep- 
tible to inflammatory affections. Another feature is offensive 
odor of the saliva of individuals who show this particular ten- 
dency to catarrhal affections even in persons who take most scru- 
pulous care of the teeth. In the majority of cases, pyorrhoea is 
a stomatitis in which the local and constitutional factors in the 
production of the disease are largely dependent upon hereditary 
catarrhal dyscrasia for their ability to engraft themselves upon 

1 American System of Dentistry. 
-' Dental Cosmos, Vol. XXVIII. 
; Sajous' Annual, 18S8, Vol. Ill, page 365. 


the tissues. This position is borne out by the clinical experience 
of Patterson, of Kansas City, Missouri, who reports thirty-eight 
cases of well marked pyorrhoea observed by him, thirty-three of 
which presented undoubted evidence of nasal catarrhal condi- 
tions ; two were the result of direct irritation of misfitting partial 
plates, and the remaining three were apparently caused by cal- 
cific deposits. Patterson remarks that a close examination of the 
history of the above quoted cases confirms the opinion that the 
disease is, as a rule, an " oral catarrh." 

From the foregoing W. X. Sudduth feels justified in class- 
ing the disease as a localized catarrhal stomatitis which may be 
either acute or chronic. Acute catarrhal inflammation of the 
gums begins in circumscribed points which present a bright or 
rose-red color, and which are generally located on the margin or 
the rugse of the palate. There is but little swelling because of 
the dense nature of the sub-epithelial connective tissues. The 
gums present the same stages as are found in inflammation of 
other mucous surfaces — first dryness, followed by an increased 
secretion of mucus. The parts are very sensitive to pressure; 
the patient complains of an annoying, burning sensation. The 
appearance of the gums is noticeably smooth and glistening. 
They bleed easily when the brush is used or even during a meal. 
This stage does not last very long, but soon heals by resolution 
or passes into a chronic catarrhal stomatitis in which condition 
the gums become markedly swollen and turgid. They present a 
condition of tumefaction that sometimes rapidly passes into 
hypertrophy ; at other times there is an indurated appearance 
that may last for some time. Granulation tissue may be pro- 
duced as the result of overstimulation. The gums become 
detached from the necks of the teeth ; and pockets are formed 
from which a fetid discharge may be pressed, giving a peculiarly 
disagreeable odor. Bulla are apt to form, which, by rupturing 
in the process of mastication, give rise to intense smarting. The 
tongue constantly seeks the surface if it be on the inner side. 

The pathologic changes which take place are, according to 
Newland Pedley, of England, "hypertrophy of the muco-peri- 
osteal fold around the teeth, accompanied by dilatation of capil- 
lary loops, enlargement of the papillae and rapid proliferation of 
epithelial cells. Later the gums become firm and contracted and 

display increase of fibrous tissue. The changes which go on in 
the socket have not been as yet satisfactorily worked out. The 
examination of the jaws of earnivora, apparently affected with 
pyorrhoea alveolaris, leads to the supposition that osteitis of the 
alveolar process spreading toward the apex of the socket is pres- 
ent. Later the alveolar walls become absorbed and are at times 
more or less denuded, while the fangs of the teeth become coated 
with a layer of thin, hard, green-brown tartar. Ultimately the 
disease progressing, the teeth, one after another, drop out." 

From what has been said it will be seen that the pathology 
of pyorrhoea alveolaris may be explained in several ways. The 
general causes are local or symptomatic, or both combined. The 
most common cause of catarrhal gingivitis is found in local 
irritation, combined with some hereditary disposition to catarrhal 
affections. The next greatest etiologic factor is symptomatic — 
the local manifestation of a constitutional vice. The most com- 
mon manifestation is that of syphilis and of its antidotes, mercury 
and potassium iodide, both of which sometimes find expression in 
a localized inflammation which may be the starting point for 
pyorrhoea alveolaris. As a complication of the disease in its 
secondary stages there can be no doubt of the action of micro- 
organisms, but Sudduth does not feel justified in conceding to 
them a position of specificity. 

His position above quoted is sustained by Pedley, who finds 
that in most instances it is due to some constitutional condition. 
The fact that it is often symmetrical and frequently hereditary 
gives support as to this view. It occurs in mouths of patients 
whose health has been undermined by debilitating influences and 
injudicious habits of living. It is a common sequel of malarial 
fever. Young persons recovering from eruptive fevers are some- 
times subjects of pyorrhoea alveolaris. Frequent pregnancies are 
a fruitful source of the disorder. Attention has been lately 
drawn to the shedding of the teeth in tabes dorsalis, but it does 
not, however, seem to be a constant symptom. Pedley 's view. 
although tending entirely toward the constitutional character of 
the disease, does not militate against its catarrhal nature. 

Bland Sutton has found shedding of teeth frequent in rheu- 
matoid arthritis in animals. He has also met with it in mollities 
ossium and other wasting diseases. Magitot (who views the 


alveolar dental periosteum as a ligament and not of the same 
nature as osseous periosteum) calls the disease symptomatic 
alveolar-arthritis, and mentions especially as causes, chronic 
Bright' s disease and glycosuria, in which latter condition the 
phenomenon is absolutely constant. 

Patterson holds that " mouth-breathing has, in his expe- 
rience, been a very common accompanying condition which he 
cannot help connecting with the production of the disease. By 
it the gums are kept dry, their functions destroyed and the way 
paved for catarrhal inflammation. The majority of the patients 
he has been called upon to treat have been otherwise healthy, 
robust persons. From this fact he does not favor the idea of the 
disease being dependent upon constitutional derangement. It 
is, however, a well-known fact that these are the very class of 
people who when irritation is once set up in their system, present 
the most aggravated cases, by reason of their superfluous vitality. 
He says he has occasionally met with cases where the local con- 
dition was evidently aggravated by constitutional derangement 
and cure was thereby retarded. The great majority of cases, 
however, have shown no indication of constitutional predisposi- 
tion, but have pointed unerringly to local irritation by means of 
which the function of the mucous membrane had been destroyed." 

Syphilis and other affections may engraft themselves upon 
the gums without a predisposition of the parts toward an inflam- 
matory condition, and having disturbed the normal status of the 
gingival margins they pave the way for subsequent disease in 
the alveolus. Certain drugs, such as mercury, phosphorus, lead,, 
etc., have a known deleterious action upon the ligamentous 
attachment of the teeth. 

In 1890 Miller 1 expressed the opinion that the disorder was 
of a parasitic nature. 

In 1892 C. N. Pierce 2 charged the disorder chiefly to sys- 
temic predisposition and enthusiastically advocated the theory of 
Reese as to the influence of the uric acid diathesis. In 1894 
W. X. Sudduth 3 strongly urged the influence of lactic acid as a 
local factor in the disorder. 

Micro-Organisms of the Human Mouth. 
International Dental Journal, Vol. XIII. 
'Ibid., Vol. XIV 

John Fitzgerald, 1 in 1899, claimed that "The production of 
pyorrhoea depends upon two factors, a predisposing cause and 
a local irritation. The predisposing cause may be tubercle, 
syphilis, scurvy, the exhaustion of acute infectious di>e;i>r> or 
any other source of malnutrition. The exciting cause may be, 
and most usually is, a gingivitis produced in one of the ways to 
be presently described. There is also a pyorrhoea of gouty 
origin, in which the local necrosis of the peridental membrane is 
caused by gouty disease of one of the blood vessels in its sub- 

The views on etiology of this condition have varied, it will 
be observed, from purely constitutional causes to purely local 
causes, inclusive of microbic affections. In the main it will 
be obvious, however, that both constitutional causes, whether 
inherited or acquired, have been regarded as of influence by the 
majority of those who have written on the subject. There has, 
however, been very little exact study of either the predisposing 
or the exciting causes of the condition. Even the impetus given 
the study of etiology by bacteriology and embryology has as yet 
failed to make itself felt to any considerable degree in this 
department of dental pathology. 

'Clinical Journal, March 1, 1899. 



The attempt has been made in the present work to reduce to 
order the chaotic notions as to etiology, pathology and treatment 
which, during the present century, have gathered around the 
morbid condition erroneously entitled Pyorrhoea Alveolaris. 
While even erroneous titles may have their meaning so fixed by 
usage that any danger from the error involved in the title may 
be practically nil, still this is not the case with the title just 
cited. It suggests erroneous etiology, since pyorrhoea implies 
that there must always be a flow of pus, and hence that the dis- 
ease must always result from infection with pus microbes. It 
implies erroneous pathology and erroneous treatment for the 
same reason. This being the case, such a title is so dangerously 
misleading as to compel in the present stage of dental science its 
complete disuse. With a view of clearing up this question at 
the outset by the use of a proper title, I have adopted as a desig- 
nation for the condition hitherto known as pyorrhoea alveolaris, 
the term "Interstitial Gingivitis." To this designation (as to all 
other attempts to express within a small space an extended path- 
ology, etiology, prognosis, and clinical aspects) there are some 
objections. The term interstitial is used by some pathologists in 
a limited obscure sense. By the mass of dental pathologists, 
surgeons, physicians, and by medical lexicographers, the term is 
employed in precisely the sense in which it is used in the present 
work. The English surgeon and lexicographer Quain defines 
interstitial as follows : " Interstitial (inter, between ; and sto, I 
stand) ; relating to the interstices of an organ. The term is 
applied in physiology to the tissue which exists between the 
proper elements of any structure, namely, some form of connect- 
ive tissue. In pathology the word is used in connection with 
absorption when a part is gradually removed without any obvious 


breaking off, and also to indicate the implication of the intersti- 
tial tissues in morbid processes or their infiltration with morbid 
products, as interstitial pneumonia, interstitial hepatitis." 

The Encyclopaedic Medical Dictionary of the American 
Foster, states that interstitial has three significations : First, it is 
applied to a condition disseminated through the substance of an 
organ or part, and to an inflammation affecting the connective 
tissue of an organ ; second, it is also applied to that form of 
growth which consists in the interposition of new elements 
between old ones, instead of in addition to the surfaces ; third, it 
is applied to pathologic processes occupying the space between 
the essential parts of an organ which constitute its proper tissue, 
and is then employed in a sense opposed to that of parenchy- 

A glance at the illustrations demonstrates the validity of the 
application of the term interstitial (in the sense of Quain, Foster, 
and the other lexicographers) to the condition erroneously called 
pyorrhoea alveolaris. 

I have adopted the term gingivitis for reasons which will be 
obvious at the first glance. The philologic objection may be 
made that in it Greek and Latin are yoked together. Practically 
this is no objection, since German, French, as well as English, 
medical authorities employ such terms of mixed origin. Indeed 
the French (Mailhol 1 for example) apply the term gingivitis to 
the very condition to which I have applied it. In addition, they 
add to it the specific term " expulsive," to designate " a form of 
recession of the gums, accompanied by alveolar osteoperiostitis, 
and the gradual expulsion of the tooth from its socket." Foster 2 
suggests the substitution of the term ulitis as more philologically 
correct. The term gingivitis, however, has crept into such wide 
use, that it would be futile to attempt to displace it for merely 
philologic reasons. The two terms I have employed convey a 
fairly correct idea of the pathologic process involved, and do 
not imply erroneous views as to etiology, pathology, prognosis 
and treatment. 

The pathologic conception adopted in the present work anent 
interstitial gingivitis is that the disorder is a local inflammatory 

1 Odontalgie. 
- Foster, op. cit. 


condition of the gums, tending to accelerate their normal ten- 
dency to disappearance at certain periods of stress, or involution, 
of which involution the changes jDroduced by old age are a type. 
In this early senility of the gums, for such it may be termed, 
two great types of causes play a part ; the exciting and the pre- 
disposing causes. The exciting causes may be purely local, or 
may be local expressions of constitutional states. Thus it will 
be shown that the influence of uric acid when present is exerted 
as a local irritant, and not as a constitutional factor — the theory 
urged so strongly by Pierce, whose views have been of late so 
advocated by Kirk. 1 The uric acid hypothesis, once very domi- 
nant in medicine, is now losing its force. The trend of medical 
opinion is to consider it one of the danger signals of auto-intoxi- 
cation which assumes prominence because of its tendency to 
excite local irritation. It is but one of a number of local 
expressions of constitutional defect. This view of the influence 
of uric acid in etiology the present work will try to demonstrate. 
Prominent among etiologic factors which have to be reckoned 
with, are pathogenic germs. In the jn-esent work it will be 
shown by all laws of bacteriology (under which investigations 
must be conducted) that there is no specific germ which is caj)a- 
ble of producing the disease itself, and furthermore, that the 
pyorrhoea stage of the disease is merely a complication due to 
pyogenic germ infection of the already diseased gums. The 
views of Galippe as to a specific organism will be shown to have 
failed of support by numerous control experiments described in 
the present work. As these have been conducted by different 
experimenters they are free from the personal elements of error 
which vitiate the researches of Galippe, who violated that canon 
of the laws of Koch which compels production of the disease by 
the alleged specific germ. One predisposing factor will be 
shown in the present work to be the nature of the structures 
affected. This in pathology is called local predisposition. The 
gums, etc., will be shown to be transitory structures in them- 
selves predestined (as already stated) to certain changes at cer- 
tain ages. By the influence of the disease, about to be discussed, 
these changes occur prematurely. The influence of the toxic 
agents (mercury, potassium iodide, etc.) will be shown to have 

1 International Dental Journal, May, 1899. 


been exerted constitutionally through the central nervous system, 
their local effects being a secondary consequence of this. The 
same will be shown to be the ease with conditions like scurvy 
(where the constitutional factor is most prominent ), and with the 
great neuroses (paretic dementia, locomotor ataxia, etc.). Here, 
as in the toxic conditions, one great element considered is the 
influence of the constitutional conditions upon the nerves gov- 
erning local blood supply and tissne waste and repair. These 
influences are significantly illustrated in the various processes 
described later which tear down and build up. 

The influence of morbid heredity as a direct factor will be 
shown nut to lie great. The influence, however, of degeneracy 
expressing itself along the lines of least resistance will appear 
as an ominously important factor. Heredity here, as elsewhere, 
is a warning rather than a destiny. 

The influence of the nervous system on the processes of 
growth and repair, which is called its trophic function, has been 
shown to play a part in both the etiology of the disease and in 
its progress. This function has received but little attention from 
dentists, albeit its influence has been recognized in dental path- 
ology in connection with great neuroses like paretic dementia 
.and locomotor ataxia, in which gum disorders occur, followed by 
loosening of the teeth. The pathology of the disease has been 
discussed in the light of established facts of general pathology 
which have been accepted by the leading dental investigators, 
and not merely from a hypothetic standpoint. The disease has 
been regarded as a local exaggeration of certain physiologic pro- 
cesses, accompanied by diminution of the intensity of others. In 
the study of this phase of the question, the latest researches of 
dental pathologists as well as original observation and experiment 
have been employed. 

Among the many questions which the present treatise is 
believed to settle (so far as experimentation can) is the following : 
The question of the influence and nature of its etiology. It is 
shown that here, as elsewhere in biology, the etiology of morbid 
conditions has many phases; that in it exciting and predisposing 
causes have alike to be considered ; that while causes may be 
constitutional in origin they very often exert their action locally ; 
that the disease is not a product of civilization nor a product of 


any one etiologic factor ; that there is no ground yet adduced 
for believing the disease to be specifically infectious and due to a 
germ of a specific nature ; that in it the germ infection occurs 
as a consequence of existing disease, and is not the cause of 
the morbid condition, but one of its stages : Pyorrhoea. The 
experiments made, as well as the pathologic and clinical data, 
have been obtained from many observers, so that as many control 
observations should be had as were necessary to eliminate per- 
sonal elements of error inevitable upon original observation and 
research. In the pathology no statement is made which is not 
demonstrated by corroboratory data, including a photograph of 
the condition. The treatment has been based upon the pathology 
and etiology. Its central idea is that the human being must be 
regarded as something more than his mouth and teeth ; hence the 
duty of the dental scientist is, like that of all medical scientists, 
best shown in a prophylactic direction. 

The pathologic material for the study of interstitial gingivitis 
in man is obtained with such difficulty in the recent state as to 
necessitate research upon animals. This disease was noticeably 
present among the carnivora, casually inspected in American 
and European zoologic gardens. Cats and dogs were also known 
to be liable to the disease. As the first step in investigation, two 
practitioners of comparative medicine, with an extensive hospital 
practice (Dr. Charles E. Sayre and Dr.. Alsop E. Flower), were 
consulted as to the frequency of this disease in animals. All 
animals under their care suffered from it more or less, but eighty 
per cent of dogs over eight years of age had the disease. Nearly 
every dog in the hospital under their care was so affected. These 
dogs comprised all breeds, from spaniels and terriers to the New- 
foundland, St, Bernard and great Dane. On examination, 
every phase of interstitial gingivitis was found in the mouths 
of these dogs, from its inception to the loss of the teeth. The 
number of dogs observed was twenty-seven. The roots of the 
teeth of some were covered with deposits and so exposed that the 
teeth could be removed with the fingers. Such diseased mouths 
are rarely, if ever, present in human beings. The outer plate of 
bone was absorbed, the roots entirely exposed, pus was oozing 
from around them and the mucous membrane was badly inflamed. 

It should be remembered that the jaw of the dog, like the jaw 



of man, is undergoing considerable variation. Like man, the 
dog, having put himself under new social conditions (so to 
speak), is varying greatly both as to brain, skull and jaw from 
his wolf-like ancestor. As he is under the protection of man, 
the struggle for existence as to food is less intense than in the 

wild state and consequently there is less occasion, even for fight- 
ing purposes, of his jaws and teeth. 

Independently of conditions of this type, many of the dogs 
suffered from constitutional disorders. Eight had skin diseases 
which in the dog are more likely to produce obvious consti- 
tutional defects than in man. Some were old and blind. Some 
had been injured and were under treatment for wounds. Some 



were suffering from rachitis, nervous diseases, and were over- 
bred. Others were constipated or had germ types of diarrhoea. 
One had kidney inflammation and bronchitis with high fever. 
In short, these dogs, being house dogs, presented most of the 
constitutional diseases to which man is liable. 

The mouth of a Scotch terrier is shown in Fig. 1. The 

molar and premolar had been removed with the fingers. The 
cuspids and incisors are quite loose. There are large deposits 
of tartar. The gum and alveolar process have been absorbed 
nearly one-half the length of the roots of the teeth. In Fig. 2 
is seen the mouth of a Boston terrier with the incisors and pre- 
molars removed. There is extensive pyorrhoea. There are 



calcic deposits upon the cuspids and molars. There is recession 
of the gums and alveolar process. In Fig. 3 is shown the mouth 
of another Boston terrier. In it one premolar in the upper and 
one on the lower jaw have been extracted. There is extensive 
inflammation of the gum about the molar, cuspid and incisor 
with large calcic deposits about the teeth. In Fig. 4 are shown 

teeth covered with calcic deposit the entire length of the root. 
These teeth were removed by the fingers from the mouths of two 
dogs, one of whom was later obtained for scientific study. This 
was all the material to be obtained from the hospital, since the 
dogs were pets who had been placed under treatment by their 



Through the courtesy of Pound master Hugh Curran, the 
necessary material was obtained from the Chicago Dog Pound. 
Here from four hundred to a thousand dogs are killed per week 
during June, July and August each year. Ninety-five per cent 
are mongrel curs leading a street life, hence neither luxu- 
rious diet nor luxurious care can be charged with any disease 
in them. They have, at least, plenty of outdoor exercise and 
fresh air. Many, despite this reversion to the life of their wolf- 
like ancestors, have skin diseases and are deaf and blind from 
old age. The bodies were secured after death, at which time 
examinations of the mouths were made. Five per cent of the 
dogs entering the pound are of good breeds. These, if not called 
for by the owners, are sold for a moderate price. 

The dogs selected for the death penalty are collected in a 
large box pen, leading out of which is a door through which they 

ff rtftftftjt* 

Fi(i. 4. 

pass into an air-tight box. Communicating with this box is a 
stove in which sulphur is burned with charcoal. The fumes 
pass into the box and death is almost instantaneous and 
painless. After they remain fifteen minutes, a door leading to 
the air is'opened and the bodies are carted away. It was at this 
time that access was had to them. The mouths were then exam- 
ined. Such cases as 'were of interest were placed on one side 
and the jaws removed from the bodies. Inside of one-half hour 
the specimens were in a solution to be kept until desired for use. 
Jaws (with interstitial gingivitis in all stages of progress, from 
simple inflammation of the gums to the most extreme cases of 
exfoliation of the teeth) were obtained in an abundance for 
future studies. It is not an easy matter to ascertain the ages of 
these animals. In a general way, it was found that inflammation 
of the gums, especially about the canine teeth, was almost always 
present in dogs over one year. About twenty-five per cent of 


these dogs at four years of age had the disease, eighty per cent at 
from eight to ten years, ninety-five per cent over twelve years of 
age. Since I commenced my investigation (four years ago), I 
have examined quite a large number of dogs about homes, but 
have never found a dog over four years without this disease to a 
greater or less extent. Many house clogs at one year had inflam- 
mation of the gums. Dogs for infection and those used for mer- 
eurialization were picked up in the streets. 

Most of the dogs exhibited at the last three animal dog shows 
held in Chicago were young, ranging from one to four years of 
age. About twenty-five per cent would range four years to 
eight. Three years ago, on a casual examination of their mouths, 
interstitial gingivitis was found to lie common. Occasionally 
recession of the gums and pyorrhoea alveolaris occurred. During 
the last two years, on more careful examination, twenty-five per 
cent of dogs between the ages of one and four were found to have 
interstitial gingivitis and seventy-five per cent of dogs from four 
to eight years were found to have interstitial gingivitis with 
recession of the gums and pyorrhoea alveolaris. In the study of 
this disease, therefore, dogs are excellent substitutes, since for 
pathologic research they can be obtained at any stage of the 



Because of man's advance in evolution and because of the 
local degeneracies thereon resultant, through the law of economy 
of growth whereby one structure is sacrificed for the benefit of 
the organism as a whole, the face, jaws, teeth, gums, alveolar 
process and peridental membrane, being variable structures, are 
predisposed to disease in their very order of evolution. 

The jaws are growing smaller because large ones are not 
required. The structures are changing their shapes to adapt 
themselves to the new environment. Thus — instead of broad 
large jaws with low vaults; short, broad alveolar processes with 
plenty of blood supply and vitality to resist mastication ; teeth 
short, with large bell crowns to give plenty of room between the 
roots for considerable thickness of the alveolar process for the 
nourishment of the peridental membrane and support and pro- 
tection of the gum tissue — small narrow jaws occur with appa- 
rently high vaults ; long, slender and thin alveolar processes, 
which are not used in mastication with sufficient force to carry 
the blood for the nourishment of the tissues. The teeth are 
changing their shape, causing the roots to come closer together, 
and thus lessening the area of the alveolar process. 

That the jaws of man are growing smaller is easily demon- 
strated by the following procedure : Drop a perpendicular line 
from the supraorbital ridge, whereupon it will be found that 
the jaws of the primitive races protrude beyond the line, as is 
the case with many peoples of Europe and Asia today. 

Mummery, on examination of the skulls of two hundred 
Britons and Roman soldiers in Hythe Church, Kent, Eng- 
land, found the narrowest width 2.12 inches, the highest 2.62, 
with an average of 2.50. The width of jaws of 402 British 
soldiers today is : narrowest 1.88 ; widest 2.63, average 2.28. 


The highest width was very rare, only eight measured '2.~>0. 
The jaws of the mound-builders compared with the existing cliff- 
dwellers show similar results, the average width is about 2.50 
inches. Measurements of normal jaws of 855 Italians of Cen- 
tral Italy were: narrowest 1.88, widest 2.63, average 2. 17. 
Measurements of normal jaws of 1,935 Americans gave the fol- 
lowing results: narrowest 1.75, widest (only one case) 2.56, aver- 
age 2.13. While in the highest type of primitive man. the 
width of the upper jaw from the outer surfaces of the first per- 
manent molars near the margin of the gum was 2.50 inches in 
diameter, the jaws of people now living in the same locality are 
from 0.25 to 0.33 of an inch smaller. The antero-posterior 
diameter has also shortened from one-half to five-eighths of an 

Standing on the corner of Picadilly Circus and Regent 
street, London, in the fall of L s< .'7. I examined the facts of 
10,000 passers-by and found that eighty-three per cent possessed 
jaws inside of the perpendicular line. Of 3,000 English school 
children under ten years of age ninety-three per cent possessed 
jaws inside of the perpendicular line, thus showing a difference 
of ten per cent in one generation. 

The negroes were formerly, in the opinion of anthropologists. 
in the main a long-headed dolichocephalic race with protruding- 
jaws. Of the Northern negroes, who in the main have white 
blood, very few have long heads. The same is true of the rela- 
tions of the jaws. The protrusion of the jaws has largely dis- 

That the jaw is becoming smaller is further shown by the 
disappearance of the third molar, or the irregularities resultant 
on its eruption because of want of room, or its eruption with 
pain for like reason. In the primitive races it is large and 
well developed. 


The alveolar processes are situated upon the superior border 
of the inferior maxilla and upon the inferior border of the 
superior maxilla. These bones, considered a part of the maxillary 
bones often so described by anatomists, should, however, be con- 
sidered as practically distinct bones — their structure, functions 


and embryology differ so completely from the structure and 
functions of the maxillary bones. The superior and inferior 
maxillae are (unlike the alveolar processes) composed of hard, 
compact bone structure. The large, powerful muscles attached 
to them indicate that powerful work is to be accomplished. 
When fully developed they retain their full size through life. 
The alveolar processes are composed of soft, spongy bone of a 
cancelloid structure. As early as the eleventh week of intra- 
uterine life, calcification of the deciduous teeth commences, and 
by the twentieth week calcific material is abundantly deposited. 
Ossification is also rapidly progressing about the dental follicles. 
At birth, the sacs are nearly or quite inclosed in their soft, bony 
crypts, and the crowns of the teeth upon their outer surface are 
composed of enamel, which is dense and hard. The embryologic 
phases of the dental shelf elsewhere cited indicate this develop- 

The alveolar process, being soft and spongy, molds itself 
about the sacs containing the crowns of the teeth and about their 
roots after their eruption, regardless of their position in the jaw. 
While the alveolar processes have grown rapidly, they have up 
to this time developed only sufficiently to cover and protect the 
follicles while calcification proceeds. When the crowns have 
become calcified and the roots have begun to take in their calcific 
material, absorption of the borders of the processes takes place in 
the order of the eruption of the teeth. When the teeth have 
erupted, the alveolar process develops downward and upward 
with the teeth until they attain the depth of the roots of the 
teeth, which extend in most instances into the maxillary bones in 
the anterior part of the mouth at least, and the upper and lower 
teeth rest at a point in harmony with the rami. The depth at 
which they penetrate the bone differs in different mouths. This 
depends upon the length of the roots and the alveolar process. 
This in turn depends upon the length of the rami. The incisive 
fossa, the canine eminence and the canine fossa give evidence of 
this externally. These sockets are lined with extensions of the 
process, thus making its upper border irregular. The crypts of 
the permanent teeth are located at the apices of the roots of the 
temporary teeth. The permanent teeth have large crowns which 
touch each other, forming a line to the posterior part of the jaw. 


These teeth, as they erupt, entirely absorb the alveolar process 
which surrounded the temporary teeth, and as the new set conies 
into place a new process is built up around them for their sup- 
port. The permanent teeth require a deeper alveolar process to 
support their roots, which are much longer than those of the 
temporary teeth. Hence the difference in the depth of the vault 
of the first and second sets of teeth. 

The alveolar process of each superior maxilla includes the 
tuberosity, and extends as far forward as the median line of the 
bone, where it articulates with the process upon the opposite side. 
It is narrow in front, and gradually enlarges until it reaches the 
tuberosity, where it becomes rounded. 

The process is composed of two plates of bones, an outer and 
an inner, which are united at intervals by septa of cancellous 
tissue. These form the alveoli for the reception of the roots of 
the teeth. In some cases the buccal and labial surfaces of the 
roots of healthy teeth extend nearly or quite through the outer 
bony plate and are covered by the peridental and mucous mem- 
branes only. 

This plate is continuous with the facial and zygomatic surfaces 
of the maxillary bone. The inner plate is thicker and stronger 
than the outer, and is fortified by the palate bones. The external 
plate is irregular upon the outer surface, prominent over the roots 
of the teeth, and depressed between the roots or interspaces. 

With the change in the size of jaws there is also change in 
the shape of the vault and alveolar processes. When the dental 
arches are large, measuring from 2.25 to 2.50 inches, the vaults 
are low and the alveolar processes are short and thick, not only 
giving stability to the teeth, but also plenty of nourishment. 
Now that the dental arches are growing smaller, with an average 
of from 1.90 to 2.00 inches, the vaults are higher in proportion, 
the alveolar processes long and thin. This renders the teeth and 
jaws more susceptible to trophic changes and hence to disease. 
The alveolar process in the anterior part of the mouth, in which 
the incisors and cuspids are situated, is much thinner than in the 
posterior parts. 

The sockets for the incisors and cuspids are conical and much 
larger than any of the other single sockets. The alveolar pro- 
cess is longer and thinner than at any of the other teeth. The 


sockets for the bicuspids are flattened upon their anterior and 
posterior surfaces, and near the apices they are frequently bifur- 
cated. The sockets of the molars are large at the openings. 
About the middle of their length, however, they are divided into 
three smaller sockets for the reception of the roots. In the case 
of the third molar the number of sockets ranges from one 
large cavity to three or four of smaller size. When disease 
attacks the tissues, destruction is, therefore, more rapid in its 
progress in the anterior parts of the mouth than in the posterior, 
where the processes are thicker and more nourishment is 

The septa are very thin at the margin and gradually increase 
in width to the middle of the jaw, where they become thicker, 
and are finally lost in the substance of the jaw. Some septa are 
thicker than others, and where two teeth are widely sepa- 
rated, the width of the septa naturally corresponds to the space 
between the teeth. 

What is true in regard to a change in the size of the jaws is 
also true in respect to the shape of the crowns of the teeth. 
While they are not growing smaller in j>roportion to the size of 
the jaws, they are changing shapes. Once they were quite well- 
shaped, giving considerable space between the roots for a thick 
alveolar process, thus rendering support to the peridental and 
mucous membranes, now the shape has changed. The proximal 
surfaces are almost straight, lessening the width and thus allow- 
ing only for a thin septum, with barely sufficient surface to support 
the tissues. 

The sockets are lined with a thin plate of compact, bony sub- 
stance, extending from the outer and inner plates of the alveolar 
process to the apex, where there are small openings for the 
entrance of the nerve and blood vessels for the nourishment of 
the teeth. 

The bony plate lias upon its inner surface the elastic periden- 
tal membrane, which acts as a cushion for the teeth, while it is 
surrounded by a spongy bone. 

The teeth are held firmly in their alveolar sockets by the rjeri- 
dental membrane. Teeth with one conical root, and those with 
two or more perpendicular roots, are retained in position by an 
exact adaptation of the tissues. Teeth having more than one 


root and those bent or irregular, receive support from all sides 
by reason of their irregularity. Fig. 5 (a section of the jaw of a 
eat) illustrates the relative position of the teeth, peridental mem- 
brane and alveolar process to each other. 

After the removal of the permanent teeth the alveolar process 
is entirely absorbed. Fig. 6 shows how the absorption takes 
place. The teeth have all been removed from the superior max- 
illa and the alveolar process has been entirely absorbed. The 

Fig. 5.— Ground Section of Jaw and Teeth of Cat. (Andrews.) 

molars on the lower jaw having been extracted, absorption of 
the alveolar process has resulted in marked contrast with the 
anterior alveolar process, which remains intact and holds the teeth 
firmly in place. It is, hence, evident from the changes which 
occur, from the first development of the teeth to their final 
extraction, that the alveolar process exists solely to protect the 
teeth in their crypts during development and after eruption. 
After the temporary teeth are in place the alveolar process; 
remains unchanged (except by gradual enlargement in harmony 
with the growth of the maxillary bones) until about the sixth 
year, when the second set appears. The crowns of the perma- 



nent teeth require more space than those of the temporary set ; 
and the alveolar process must necessarily enlarge to accom- 
modate them. This enlargement of the alveolar process is 
caused chiefly by formation of the crowns of the permanent 
teeth before eruption, and to a limited extent only by growth of 

the maxillary bones. These may cease development at any 
period of the life of the individual, or continue as late as the 
thirty-sixth year. As diameter of the crowns of the permanent 
teeth form a larger circle than that of the maxillary bones, the 

alveolar process must necessarily increase its diameter and pre- 
sent large spaces between the roots of the teeth for the devel- 
opment of the alveolar process. 

The process is solely for retaining the teeth, and if for any 
reason the dental follicles should not be present, and the tooth 


should not erupt, or if it should be extracted early, the process 
would not be developed at that point. In my collection of 
models are cases of arrested development of the alveolar process, 
caused by the lack of bicuspid and lateral incisor germs, and by 
extraction of deciduous and permanent teeth. 

If one or more teeth were not to antagonize, the alveolar 
process would extend beyond the natural border, carrying the 
teeth with it. A marked illustration of this is seen where the 
molars are decayed to the gum and the roots remain. The vas- 
cularity of the process may be such that hypertrophy results. 
Excessive development of the alveolar process is frequently 
observed by every practitioner in connection with the anterior 
inferior teeth. When the articulation is normal, occlusion of 
these teeth never takes place. Frequently (especially in patients 
from six to twelve years of age) these teeth extend to and 
occlude with the mucous membrane of the hard palate. Such a 
case is illustrated in Fig. 7. This model is taken from the jaw 
of a person thirty-seven years of age, but this excessive develop- 
ment took place between the ages of six and twelve years, since 
at that period the vascularity of the tissues is more vigorous, and 
the development of the process more formative than at any 
period subsequent to the development of the first permanent 

In one case under, observation the incisors and cuspids, 
together with their alveolar process, are situated upon the 
external surface, while the biscupids, molars and their alveolar 
process are located upon the inner border of the jaw. In 
another case, the alveolar process failed to cover the roots of the 
biscuspids and molars upon the outer surface, the teeth having 
forced themselves into a larger circle through the alveolar process 
by the contact of the crowns. The roots in this case can easily 
be outlined by the finger through the mucous membrane, the 
outer plate of the alveolar process barely, if at all, covering them. 
Tomes 1 illustrates a case of faulty development of the outer 
plate of the alveolar process, exposing the crown of the tem- 
porary teeth. This occurred in a hydrocephalic. I have a 
number of models showing the anterior alveolar process project- 
ing beyond the normal position through the forward movement 

1 Dental Surgery, page 44. 


of the molars. This may be due to a natural movement of the 
molars forward, or the process may be forced forward by the 
improper occlusion of the jaws. The teeth are moved from one 
position to another simply by the force consequent upon absorp- 
tion and deposition of bone. This is noticeable in the sjmces 
between the centrals, when the alveolar process develops to a 
larger circle than is necessary to accommodate the teeth. The 
alveolar processes are influenced in one direction or the other by 
the pressure of articulation. This results from inharmonious 
development of the jaws. The teeth may come together in such 
a manner as to throw the alveolar processes either to the right or 
the left, thus producing a full, round arch upon one side of the 
jaws, and a perfectly flat or straight arch upon the other. Occa- 
sionally both upper and lower alveolar processes are carried for- 
ward in the same manner. The alveolar process upon the lower 
jaw is more liable to be found upon the inner border of the jaw 
than is the upper alveolar process, as the inferior maxilla is 
larger and more dense than the superior, and when the teeth are 
once in position upon the lower jaw they are not so liable to 
subsequent change. Owing to this the teeth of the superior 
maxilla do not form so great a circle. This causes the teeth 
upon the sides of the jaw to conflict, and the lower teeth and 
alveolar processes to be carried in, while the anterior teeth of the 
lower jaw are held inside of the superior anterior teeth, thus car- 
rying the alveolar processes inward. 

The teeth are continually changing their positions in the 
mouth. This is as often beneficial as it is detrimental. That the 
teeth may perform their full function, they should not only 
remain firmly in the alveolar process, but they should also antag- 
onize properly. The teeth may be compared to the bricks in an 
arch. Remove a brick and the arch falls to pieces. It is fre- 
quently found that the teeth do not articulate properly ; by a 
slight movement, or by cutting away the grinding surfaces, a 
better articulation may be secured. When this operation is per- 
formed, the teeth move in their sockets by absorption and depo- 
sition of bone, demonstrating the fact that the process changes in 
shape and substance. Ziegler 1 says absence of functional use is 
a, frequent cause of premature lacunar absolution of the bone. 

1 A Text-Book of Sj^ecial Pathological Anatomy, page 145. 


This form of atrophy from disuse occurs not only when a limb or 
a part of a limb is deprived of its normal activity, but also when 
portions of a single hone cease to perform their function of sup- 
port, and finally, like all the hones of the body, as age advances. 
normal or physiologic absorption takes place, while the teeth are 
still in the jaws. Unlike other bones of the body, however, the 
absorption of the alveolus progresses to a greater extent because 
of the unstable condition of the structures. 

From what has already been said of the vascularity of the 
alveolar process, it is evident that hypertrophy of the tissue may 

ensue from an unbalanced nervous system and from simple irri- 
tation of varying degree. The irritation consequent upon the 
eruption of the teeth, together with the excessive blood supply, 
are both primal causes of overbuilding of tissue, i. e., hyperplasia. 

The ragged roots of the temporary teeth, produced by absorp- 
tion of the gases from the putrescent pulps, and the pressure of 
the permanent crowns against the tissues, produce sufficient 
stimulation to excite physiological action. Tissue-building gener- 
ally is seen in connection with all the teeth, and the process 
becomes unnaturally thick, the teeth frequently are carried in 
one direction and another; cementosis of the roots of the teeth 
and hypertrophy of the process result. 

In cases of hypertrophy of the alveolar process, enlargement 
is associated with the inner plate of the alveolar process. In 
cases coming under my observation the inner plate in most is the 


part of the alveolar process affected (Fig. 8 case). The outer 
plate, although quite irregular from the arrangement of the teeth, 
is usually normal in thickness. This disparity in the two plates 
of the alveolar process is clue to the fact that the inner plate of 
the alveolar process possesses a large blood supply, the posterior 
or descending palatine arteries furnishing the ossific material. I 
have observed but few cases where hypertrophy has extended to 
and included the outer plate. When the outer plate becomes 
involved the alveolar process assumes a very thick condition. 
Occasionally hypertrophy will affect one side only or one distinct 

locality (Fig. 9). In this case the enlargement is upon the left 
side and extends from the first bicuspid posterior to and including 
the maxillary tuberosity. Instead of the force being directed 
inward, as is generally the case, the process is forced outward and 
backward. This enlargement occurred previously to the develop- 
ment of the second and third molars. The alveolar process 
extends downward and occludes with the teeth upon the lower 
jaw, thus preventing the molars from erupting. 

Under the microscope, two systems of Haversian canals are 
seen in the alveolar process. Kolliker 1 describes these as follows : 

"The Haversian canals are of two kinds. One with the 
regular lamella? system surrounding it, and the other, the so-called 

1 Handbuch der Gewebelehre, page 272. 


Volkmann's canals, containing the perforating vessels from Yon 
Ebner, which have no surrounding lamellae, but simply penetrate 
through the layers of bone. Volkmann's canals are present in 
all tubular bones in old and young. While especially present in 
the outer basal lamellae, they occur also in the interstitial leaflets 
and in the inner chief lamellae as well as in the periosteal layers 
of the skull bone. Here their number is very variable (Fig. 10). 
They run partly transversely or obliquely, and also partly longi- 
tudinally, through the lamellae. Many of these canals open in 

Fig. 10. — Section of Bone Showing Blood Vessels of Von Ebner. 

the outer or inner surfaces of the substantia (compact substance), 
and also here and there in the Haversian canals, and form alto- 
gether usually a wide-meshed irregular network. In their struc- 
ture they are sometimes smooth and sometimes furnished with 
dilatations and angles projecting in and out in profile. The 
widest has a diameter of 100 micrometers or more, and the 
narrowest not more than 10 or 20 micrometers, and there are still 
narrower ones which are altogether obliterated, appearing like 
rings or circular-formed structures without any lumen, or like 
those far from rare obliterated true Haversian canals first 
described by Tomes and de Morgan. The contents of the 
Yolkmann canals are the same as the Haversian canals." 

Fig. 1() is a cross section of the medulla of a calcined human 



"humerus slightly enlarged. The outer lamellae contains a large 
number of Volkmann's canals running longitudinally and trans- 
versely and extending through the outer plate of bone into the 
periosteum. Fig. 11, the cross section of the section seen in 
"Fig. 10, shows these canals more highly magnified. The Haver- 
sian canals are large round spaces (Fig. 12), containing a single 
artery and vein. The fine hair-like spaces running from these 
large spaces are the canaliculi. The dark spots circulating each 
Haversian canal are the lacuna?. The canaliculi run from one 
lacunae to another or into a Haversian canal or they anastomose 
-with each other. The rings of bone about each Haversian canal 
.are called lamellae. The lacunas seem to be about uniformly 

: - r ---2rc e° 

Fig. 11.— Section of Bone (Higher Magnification) Showinq Blood Vessels of 
Von Ebnkr. 

■distributed throughout the bone. The spaces between the 
lacunae and canaliculi are filled with lime salts. 

A longitudinal section of bone (Fig. 13) is similar in appear- 
ance to the cross section. Instead of the lacunae being arranged 
in rows around the Haversian canals they are parallel. It will 
be noticed that the Haversian canals run in different directions 
and communicate with each other at certain intervals. The 


foregoing description, with illustrations from Kolliker, is essen- 
tially that of the minute anatomy of the alveolar process. 


The periosteum is a fibrous tissue covering the outer surface 
of the alveolus. The peridental membrane is composed of 
similar structures covering the roots of the teeth and lining 

-^SBfejl * '» 

Tig. 12. — Transverse Section of the Diaphysis of the Humerus Magnified 350 


a, Haversian Canal. Dark spaces, Lacunar. Hair-like spaces, Canaliculi. 

the inner wall of the alveolus. They are both derived from 
the mesoblastic layer. For this reason there can be very little 
difference in the character of the structure of each, except so far 
as function is concerned. The periosteum is made up of four 
different kinds of fibers. An outer layer of coarse, white fibrous 
tissue, an inner layer of fine, white fibrous tissue, elastic fibers, 
and penetrating fibers (fibers of Sharpey). 

The fibers of the periosteum are coarser than those of the 
peridental membrane. The coarser fibers run parallel with the 



alveolar process (J) over the border and extend as far as the 
union of the epithelial layer (E) and the periosteum (H), Fig. 
14. ("The dental ligament," Black. 1 ) The finer fibers run in 
all directions and enter the alveolar process at every point. If a 
section of the alveolar process treated with acids or a section 
affected by halisteresis or osteomalacia be placed under the 
microscope, the fibers are seen to retain the original shape of 
the bone. 

The fibers of the periosteum, therefore, are continued 
throughout the process from the periosteum on the one side 

fob I0m,i! 

Fig. 13. — Longitudinal Section of Bone Magnified 100 Times. 
a, Haversian Canals. 6, Lacunae seen from the side, c, Canaliculi. 

to the peridental membrane on the other. This is also illus- 
trated in the mouths of persons, where (after wearing artificial 
dentures for a short time) heat produces absorption of the lime 
salts, leaving the fibrous tissues intact. 

The periosteum is abundantly supplied with blood vessels 
which anastomose with each other and enter the alveolar process, 
at the Haversian canals. The plexus of blood vessels is much 

1 American System of Dentistry, page 663. 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 14. — Longitcdinal Section of Tooth, Alveolar Process, Peridental Membrane ani 
Periosteum. Normal Tissue. Sheep. 

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. 
H, Periosteum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, Fibrous 
Tissue. AA, Point of union of epithelial tissue and peridental membrane. 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 15. — Cross Section of Tooth, Alveolae Process, Peridental Membrane and 
Periosteum. Normal Tissue. Dog. 

B, Dentine. C, Cementum. D, Pulp. H, Periosteum. J, Alveolar Process. 
K, Capillaries. M, Fibrous Tissue. U, Nerve Tissue. C T, Connective Tissue. 



larger proportionately in connection with the alveolar process 
than with other bones of the body, owing to its transitory 

The peridental membrane commences at the margin of the 
epithelium at the neck of the tooth AA, Fig. 14, and is attached 
directly to the cementum. This membrane has various func- 
tions: First, it fills the space between these two structures, 
forming a cushion for the teeth to rest upon ; second, like the 
alveolar process, it is present only when the teeth are present, 
and therefore develops with the alveolar process when the first 
teeth erupt, it is entirely lost when the temporary teeth are shed, 
is restored with the eruption of the second set, and when the per- 
manent teeth are extracted it disappears with the alveolar process 
completely; third, it furnishes the nourishment for the teeth 
while they are in position in the jaw, and holds them in their 

The fibrous tissue, in its earliest stages comprises nearly all 
or quite all of that portion of the jaw which eventually becomes 
the alveolar process. Calcification begins at the center of the 
jaws and gradually closes in upon the fibrous membrane until it 
becomes the thickness of a sheet of paper. In young persons 
the membrane is much thicker than in old age, since, as age 
advances, the osteoblasts on the one hand and the cementoblasts 
on the other send out new material and each wall closes in upon 
the membrane, which becomes very thin in old age and almost lost. 

The fibers which compose this membrane extend in all direc- 
tions ; some crosswise penetrating the cementum, on the one 
hand, and the alveolar process on the other. In a general way, 
since the fibers extend through the alveolar wall, they are more 
closely adherent to the bone than to the cementum, and usually 
cling to the latter when the tooth is removed. It will be observed 
that these fibers do not enter the alveolar process uniformly as 
claimed by Gray 1 and Pierce 2 , like tacks or nails driven regularly 
into a board (the "fibers of Sharpey " Fig. 14), but vary as to 
quantity in different localities. In some localities they penetrate 
in large quantities and almost surround a piece of alveolar pro- 
cess, while a few fibers penetrate but a short distance. In some 


American System of Dentistry, page i 


places, the) 7 can be traced almost through the alveolar process. 
These fibers are much finer in man (Fig. 15) than in the lower 
animals (Fig. 14, dog). In connection with the fibers which pass 
into the alveolar process are numerous blood vessels. Others run 
diagonally, and still others lengthwise, all making up a tissue 
which holds the tooth in position in the jaw. The fibers enter 
the peridental membrane at all points of the process, from its 
margin to the apex of the roots. The elasticity of this membrane 
is so great that in correcting irregularities a tooth may be turned 
from one-fourth to one-half around without breaking the fibers. 
The elasticity is greatest in youth. As age advances, the mem- 
brane grows thinner and thinner until, late in life, there is almost 
a bony union between the tooth and the alveolar process, thus 
preventing stretching of the fibers. At the upper border, under 
the gum tissue, these filters extend over the edge of the alveolar 
border and unite with the fibers of the periosteum on the outer 
border of the process, forming the interstitial tissue. 

If absorption of the inorganic substance of the alveolar pro- 
cess occurs, the fibrous tissue retains the shape of the process. 
The same results when inflammation of the peridental membrane 
takes place at the gum margin or at the apex of the root of the 
tooth. What was once alveolar process is now peridental mem- 
brane or fibrous tissue. 

Two kinds of structures are present in the alveolar process — 
a dense, compact, hard structure (composed of lime salts), and a 
fibrous tissue ; either alone will retain the shape of the tissue. 

Blood vessels permeate this membrane throughout from the 
gum tissue at the neck of the tooth, through the alveolar walls 
to the end of the roots. They are most abundant in youth. 
Capillary blood vessels enter the Haversian canals through the 
process and into the cementum. Many of these blood vessels 
extend the entire length from the gum margin to the apex in 
straight lines and vice versa, In many of the illustrations, the 
blood vessels will be seen to follow the line of the alveolar pro- 
cess (Fig. 14). A great supply of blood vessels penetrate the 
membrane through the alveolar walls. These vessels unite and 
anastomose with the arteries which traverse lengthwise, forming 
a complicated plexus (Fig. 16). According to some writers the 
vascular supply of the peridental membrane is situated in the 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 16.— Cross Section of Tooth, Alveolar Process and Peridental Membrane. 
Injected Blood Vessels. Normal. Doc 

B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. K, Capillaries. 
L, Haversian Canals. 

Micro-photographs, reduced one-third. 

Fig. 17.-Ce 
B, Dentine. C, Cementum 

Section of Tooth, Alveolar Process and Peridental Membrane. 
Injected Blood Vessels. Normal. Dog. 

I, Peridental Membrane. J, Alveolar Process. K, Capillaries. 
L, Haversian Canals. 


center of the structure. This has not been my experience. All 
of my slides, as well as those here presented, show the blood 
vessels to be situated nearest the alveolar process. It is quite 
natural that this should be so, since very little blood is required 
for the nourishment of the cementum, while the largest amount 
is required to supply the alveolar process. The system of blood 
vessels situated in the peridental membrane and showing their 
relation to the surrounding tissue is well shown in the injected 
specimen from healthy dogs (Figs. 16 and 17). Pus pockets and 
abscesses are hence more liable to form near and in the alveolar 
process than near the tooth structure. When infection takes 
place, the products of inflammation are carried through the 
blood vessels and the foci of round cell inflammation are located 
near or in the alveolar process where abscesses form. The vessels 
seen in the membrane anastomose very freely with those at the 
gum margin, showing the membrane to be well nourished in all 
its parts. Should one part become involved by disease the other 
parts are overnourished in consequence. 

These blood vessels enter the alveolar walls with the fibrous 
tissue through the Haversian canals and these in turn permeate 
the entire bone. As age advances, however, the bone becomes 
more dense, and the Haversian canals become smaller and (under 
certain conditions) cease to exist. When disease takes place, 
either at the gingivus or at the apex of the root, the supply of 
blood being thus cut off, the tissues receive sufficient nourishment 
through the alveolar wall. Since the structures are in a transi- 
tory state, being destroyed and repaired so frequently, it is evi- 
dent why the blood supply is so rich. 


Small, hard bodies are frequently found in the peridental 
membrane. These are sometimes in the form of concentric rings 
of lime salts and are called calcospherites. They are not always 
round, but may be of any shape and vary as well in size. They 
bear the same relation to the peridental membrane that pulp 
stones do to the dental pulp. Black 1 says: " I have seen more of 
them about the roots of the molars than elsewhere, but have 
found them along the sides of the roots of the bicuspids."' 

1 Periosteum and Peridental Membrane, Page 94. 


When irritation and inflammation take place in the peridental 
membrane, the cementoblasts build up cement substance, just as 
the osteoblasts do in the alveolar process and the odontoblasts do 
in the pulp chamber. Sometimes they are attached to the root 
of the tooth, which produces what is called exostosis or cemen- 
tosis. They may remain unattached, floating in the fibrous tissue. 
These are very common in connection with interstitial gingivitis. 


The tooth, according to Minot, 1 is a papilla which projects 
into the epidermis, and ossifying in a particular way, changes into 
ivory around the soft core or pulp. To the papilla the e]:>idermis 
adds a layer of enamel. The tooth proper unites with a small 
plate of dermal bone at its base. By a modification on the jaw, 
the epidermis first grows into the dermis, and then the dermal 
tooth papilla is developed. The teeth were primitively organs of 
the skin and widely developed over the surfaces of the body. As 
the mucous membrane is practically a continuation of the skin, it, 
in accordance with the law of individuation, became specialized 
and lost some of the functions of the skin while developing the 
others to greater j)erfection. 

The mucous membrane lines the cavity of the mouth, the 
nose, and extends through the larynx into the lungs and through 
the oesophagus into the stomach. It covers the tongue, jaws, 
alveolar process, dipping down between the necks of the teeth 
and the alveolar process as far as the peridental membrane, leav- 
ing a free space between the membrane and the teeth through its 
entire length. 

It consists of two layers (Fig. 18), the epithelium (A) and 
corium (B), separated by the basement membrane (C). The 
epithelium is composed of the epithelial cells : First, one row of 
columnar cells (B) situated upon the basement membrane (C); 
second, two rows of six-sided prickle shells (E); third, two rows 
of six-sided cells (F); fourth, two or three rows of squamous 
cells (G) ; and fifth, four or five rows of flattened dead cells (H), 
which were originally the columnar cells upon the basement 
membrane. The young new cells are the columnar cells which 
pass from one stage to another, changing their shapes until they 

1 Embryology, page 481. 



eventually become dead cells and are exfoliated from the surface 
of the tissue. The basement membrane (C ) is made up of fibers 
running longitudinally, from papillae, which allow the tunica 
propria containing blood vessels and nerves to pass up into the 
epithelium structure. 

The corium (B) (which lies below the basement membrane ) 
is composed of alveolar connective tissue, white yellow fibrous 
connective tissue, muscular fibers, nerves, blood vessels and 
lymphatics. It is made up of the tunica propria and the 

Fig. 18. — Diagrammatic Illustration of the Epithelium and Submucous Layers or the 
Mi cous Membrane. 
A, Epithelium. B, Corium. C, Basement Membrane. D, Columna Cells. E, Prickle 
Cells. F~ Six-sided Cells. G, Squamous Cells. H, Flattened Dead Cells. 

The tunica propria (beautifully shown in Fig. 1 ( .») con>i~t~ 
of interlacing connecting fibers interspersed with much elastic 
fibrous tissue. This tissue penetrates the epithelial layer in the 


form of cone-shaped papilla;, varying in length with the thick- 
ness of the epithelium. This layer being the thickest at the 
gum margin (E), these papillae are the longest and largest at this 
locality. The fibers of the tunica propria pass gradually into 
the submucous membrane (G), and from there into the perios- 
teum and peridental membrane (M), so that it is difficult to 
determine the mucous capacity line of demarcation separating the 
different structures. The submucosa is composed of fibrous 
connective tissue of a much less compact variety. This structure 
is attached to the bones through the periosteum and peridental 
membrane. In this structure the glands, blood vessels, nerves, 
fat cells, etc., occur. 

The larger blood vessels (K) are found in this structure. 
From these large blood vessels small capillaries extend to the 
tunica propria. It is here that inflammation commences in 
interstitial gingivitis. Numerous veins accompany each artery, 
and lymphatics form a network around them. Small nerve 
filaments are also in this structure, which pass through the tunica 
propria and into each papilla in connection with the capillaries. 
The terminal nerve fibers come in contact with the muscular 
fibers, so that there is direct communication by blood vessel and 
nerve throughout the mucous membrane from the nose, stomach 
and lungs. The gum tissue is very thick and made up of fibrous 
tissue running in three or four directions, rendering it dense, 
tough and hard. The membrane thus differs from the same 
structure in other parts of the body. On account of these 
numerous fibers, this structure is bound tightly to the alveolar 
j)rocess. The gum tissue acts as a cushion and protection from 
irritation which may arise from hard substances being taken into 
the mouth. As this membrane passes and coalesces with the 
membrane of the lips and cheeks, it becomes much thinner and 
less dense. In the center of the tooth, the parallel fibers in the 
tunica propria are composed of flattened fasciculi of connective 
tissue. There are three sets of fibers — those which run verti- 
cally, those which radiate and are fan-shaped, and those which 
are horizontal. 

The mucous membrane, like the alveolar process and peri- 
dental membrane, is composed of very unstable tissue. It 
changes its structure, blood vessels and nerve system as often 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
Fig. 19. — Longitudinal Section of Tooth and Gum Tissue. 


D, Dentine. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. M, Fibrous 
Tissue. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peridental 
Membrane. RR, Space Pocket from Want of Union of the Epithelial Fold. 


as the other structures. Its blood vessels and nerve system are 
continually renewing connective tissue, periosteum and peridental 

A difference is noticed in the structure of the papillary layer 
in man and the lower animals, such as the dog, the sheep and 
the calf. In man the gum tissue is not so thick, therefore the 
papilla? are broader and shorter, while in the loAver animals the 
papillae are narrow, long and more closely set together. Blood 
vessels and nerves are not so numerous and close together in man 
as in animals. 


A somewhat widespread opinion locates special glands in the 
gingival tissues and the peridental membrane. This seems, to a 
certain extent, to be in part due to the lack of definite knowl- 
edge as to the etiology of interstitial gingivitis, and in part to the 
fact that certain constitutional conditions, such as mercurial and 
potassium iodide poisoning and scurvy, manifest themselves in 
the gum tissue in a way similarly to their action in the glandular 
structures of the body. Black 1 claims, for example : " That part 
of the gingival margin that lies in against the neck of the tooth 
is of a different structure from its other parts. Here it is clothed 
with a very soft, round or polygonal gland-like epithelium that 
suggests the formation of a gland, but fails to assume the 
glandular structure, though it seems to have been regarded as 
such by Serres. This — which I shall call the gingival organ — 
emits a profusion of small rounded cells which are always found 
in the saliva (Salter) and are usually called mucous-corpuscles. 
It is well known that certain glands have the power of the selec- 
tion and excretion of certain j)oisons, and in this way of elimi- 
nating them from the system, and that if the substance be in 
large amount, hyperemia, or even inflammation, may result. It 
is also known that mercury and potassium iodide will produce 
inflammation of the free margins of the gums, and Salter has 
found that these cells are in greater abundance under these cir- 
cumstances ; also that the cells taken from the gingival border 

American System of Dentistry, pages 955-956. 

Fig. 20.- 

>. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
-Longitudinal Section of Gum. Normal Tissue. Sheep. 

C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. 
M, Fibrous Tissue. AA, Point of T'nion of Epithelial Tissue and Peridental Membrane. 
Nm, Naysmith's Membrane. Sg, So-called Glands of Serres. 


and submitted to chemical tests after the person has taken potas- 
sium iodide, are found to yield, and are tinged with, iodin." 

Longitudinal sections of the tooth, alveolus and surrounding 
tissues, under the microscope, exhibit a very peculiar formation 
of the mucous membrane at its line of union with the peri- 
dental membrane at the neck of the tooth. Black ' (in an 
article beautifully illustrated by Frederick Noyes) seems to 
identify these with the so-called glands of Serres, or gingival 
glands (Fig. 20). He speaks of them as glands in various 
places throughout the article ; for example, " But little can now 
be said of the function of the network of glands of the periden- 
tal membrane, beyond what is indicated by their form, location 
and histological characters. With the knowledge of their posi- 
tion and general character, clinical observation leads to the con- 
clusion that they are readily disturbed by certain drugs, notably 
by mercury and iodin ; and that they are often disturbed by 
.substances poisonous to them floating in the blood streams. This 
is evidenced by the appearance of marginal gingivitis, with 
soreness of the peridental membrane. Such disturbances would 
not be likely to occur without the presence of some specialized or 
secretory tissue. ... It seems to me very certain that the 
disease which I have described as phagedenic 2>ericementitis has 
its seat' in these glands." Black, however, does not seem quite 
certain of the validity of his position, since he further remarks, 
" Though definitely lobulated, this body does not seem to jwssess 
the characters of a gland, and I should not suppose from an 
examination of its tissues that it had a glandular function. It 
encircles but a portion of the neck of the tooth, usually only the 
approximal portion, thinning away toward the buccal and 
lingual, so that in many of the lengthwise sections it may be 
very small, or does not appear at all." 

In many slides of sections from canine jaws and human, 2 the 
same peculiar arrangement of structure was observed, although 
not in so marked a degree. In the immature herbivora (calf and 

1 Dental Cosmos, February, 1899. 

2 The material obtained for making slides from man, other than the scurvy cases, 
■was obtained through the kindness of surgeons from jaws removed from hospital 
patients, as a result of disease ; the surgeons placing them into alcohol or Muller's 
solution as soon as removed. 

X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 

Fig. 21. — Cross Section of Tooth and Peridental Membrane. Normal Tissue. Sheep. 

C, Cementuni. D, Dentine. I, Peridental Membrane. W, Epithelial Debris 

X 300. No. 2 projection ocular. D. D. obj. Zeiss. Micro-photographs, reduced one-third. 
Fig. 22. — Cross Section of Tooth and Peridental Membrane. Normal Tissue. Shi 
C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 



Lamb) these peculiar formations of structure art' well marked, 
albeit less so in the carnivora, and still less in man. 

Were glands present in this locality it is logical to infer that 
they would become involved in mereurialism, plumbism and 
scurvy, and exhibit marked inflammation with broken-down 
structures in a given locality, as at the union of the gum tissue 
with the peridental membrane. Such a case is unknown. 

The mucous membrane tinder the microscope appears at a 
point between the teeth (and faintly so at the inner and outer 
border as shown by Black) to double upon itself. When the 
tooth erupts, absorption of the gums occurs at the highest point. 
The gum tissue passing down to the neck of the tooth folds or 
crowds upon itself between the teeth with a peculiar curve 
downward, inward and then outward and upward. At the 
upper border, about midway from the gingival margin to the 
neck of the tooth, may be seen a space or pocket (never twice 
alike in appearance) where the edge of the gum tissue comes in 
contact with the original epithelium. Sometimes the space or 
pocket is closed up (Figs. 43, 44, 51). Again it remains open 
(Figs. 19, 32, 50, 53). Frequently this peculiar type of 
structure is absent, showing that the fold of gum tissue either 
has been absorbed in the eruption of the tooth or did not form. 
This peculiar form encircles only a portion of the neck of the 
tooth (according to Black's examination of the structure in 
sheep). This in itself seems to oflsel the glandular theory, since 
gingivitis almost invariably starts on the lingual or palatine and 
labial surfaces where this structure does not appear. In the 
slides of the scurvy case there does not appear the slightest 
evidence of anything resembling glandular structure. Hence 
it would seem safe to conclude that the glandular structure does 
not occur in this locality. It is by no means impossible that in 
the peculiar epithelium in this locality, epithelial cells undergo 
changes which to some observers simulate glandular structure, 
but on histologic analysis are distinguishable from it, resembling 
in this the crypts of the head of the penis. 

In cross sections of the peridental membrane, with a low 
power may be seen dark bodies arranged along the margin of the 
cementum in the peridental membrane (Fig. 21). They are 
more numerous, however, near the gingival border than at the 



root extremity. These bodies are more numerous and better 
defined in the sheep than in the calf, and more apparent in the 
canine jaw than in the human. Under higher power (Fig. 22) 
they may be distinctly demarcated as epithelial cells arranged 

. wclfth obj. Zeis 

Fin. 23. — Cross Section of Tooth and Peridental Membrane. Normal Tissue. 

C, Cementurn. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 

in single rows of loops, again in double rows, again in rows of 
three and sometimes in round or oblong groups, with clusters of 
cells without shape or form. With a still higher magnifying 
power (Fig. 23) it will be seen that these masses of cells are 
polygonous, never prismatic. They hence are similar in shape 


to the epithelial cells situated above the columnar cells. They 
also resemble the cells which are situated inside of the epithelial 
lamina. In the larger amplification the nucleus can be readily 

Black 1 has attempted to demonstrate that glands exist in 
the structure and that the cells last mentioned are glands. 
Black lays down as a sine qua non of a gland that there should 
be an opening to the surface. He has made an attempt (Fig. 15) 
to demonstrate such an outlet, but this figure does not show 
clearly that the glands empty into the duct or have an exit at 
the surface. These bodies, however, not only fail (like the 
ductless glands) in this particular, but in more important 
characteristics of glands. They do not have (as Robin and 
Magitot remark) a columnar or prismatic cell wall. It is not 
difficult to understand how epithelial cells are scattered in dif- 
ferent shapes and sizes throughout the peridental membrane. 
Epithelial cells have the property of multiplying and develop- 
ing in structures wherever located. 2 

If epithelial cells should migrate within the submucous mem- 
brane and fibrous tissue, proliferation will occur under certain 
circumstances. The tooth, according to Minot, 3 is a papilla 
which projects into the epidermis and, ossifying (calcifying) in a 
particular way, changes into ivory around the soft core or pulp ; 
to the papilla the epidermis adds a layer of enamel. The tooth 
proper unites with a small plate of dermal bones at its base. By 
a modification in the jaws the epidermis first grows into the der- 
mis and then the dermal tooth papilla is developed. The first 
indication of the development of tooth germs in mammals is a 
thickening of the epithelium covering the jaw. This thickening, 
which appears as a ridge during the sixth week of embryonic 
life, forms on the under side of the epithelium. This curving 
ridge expands into an outer portion (the outline of the groove 
between the lip and the gum) and an inner portion, the dental 
shelf which grows obliquely inward. The papillae for the milk 
teeth are formed on the under side of the shelf, and it is thus 
possible for the shelf to continue growing toward the lingual 

1 Dental Cosmos, February, 1899, pages 112-118. 
-'Dental Follicle, page 116. 
•Embryology, pages 581-90. 


side, so that the second set of germs is developed for the perma- 
nent teeth. The end of the shelf, toward the articulation of the 
jaws, is prolonged without retaining the direct connection with 
the epithelium and from this prolongation arise the enamel 
organs for the three permanent molars. Wherever a tooth-germ 
arises the dental shelf is locally enlarged, and the local enlarge- 
ment constitutes an enamel organ which projects from the under 
side of the shelf. The portions of the shelf between the enamel 
organs gradually break up, forming first an irregular network, 
and later separate fragments ' which may persist throughout 
life and lead to various pathological structures. While the per- 
manent germs are forming, the shelf is solid between them, 
although it has assumed the reticulate structure between the 
germs of the milk teeth. In consequence of the reticular forma- 
tion, the fully developed enamel organs have several bands or 
threads by which they are connected with the dental shelf proper. 

After the shelf has developed somewhat, its line of connection 
with the epithelium of the gum becomes marked by a superficial 
groove, as may be seen in the human embryo of eight to ten 
weeks. This groove was formerly supposed to be the first trace of 
the dental shelf, but Rose's observations correct the supposition. 

The second step in mammals is the formation of outgrowths 
(in man ten in each jaw) from the under side of the dental shelf; 
each outgrowth is the outline of an enamel organ for a milk 
tooth. The outgrowth is covered toward the mesoderm by a layer 
of the epidermis, while the core is filled with polygonal cells 
which resemble those of the middle part of the Malpighian layer 
of the skin. The outgrowths, after penetrating a short distance, 
expand at the lower ends, but remain each connected by a nar- 
row neck with the overlying ej^idermis. The expanded end is 
the enamel germ proper ; it very soon assumes a triangular out- 
line, as seen in sections, owing to the flattening of its under side, 
and at the same time it moves somewhat toward the lips. Mean- 
while the shelf continues growing on the lingual side of each 
ingrowth to produce the enamel organs destined for the second 
or permanent teeth. 

At this stage it is noticed that the mesenchyma under the 
flattened end of the enamel organ has become more dense, to 

Including the epithelial debris of Robin and Magitot. 


form the outline of the dental papilla, and is beginning to develop 
fibrillse around both the enamel germ and the papillary outline. 
The fibrillar envelope is the future dental follicle. 

The third step is a final differentiation of the enamel organ 
and the accompanying shaping of the papilla. The enamel 
organ continues growing and becomes concave on its under side 
.so that the mesoderm underneath acquires the shape of the 
papilla. It is now that the form of the tooth is determined by 
the form assumed by the papilla, which in its turn is probably 
determined by the growth of the enamel organ. 

The follicle is merely an envelope of connective tissue in 
which can be distinguished an outer dense and inner looser 
layer; in the latter the cells are more distinct and the fibrillar 
are less numerous than in the former. A rich network of capil- 
lary vessels is developed in the follicle and appears in part as a 
series of villous-like growth into the enamel organ. The follicle 
develops first over the lower part of the papilla, then over the 
enamel organ, the neck of which aborts and the follicle closes 
over, completely separating the enamel organ from its parent 
epidermis. The enamel organ changes greatly in appearance. 
The layer of cylinder cells is well preserved over the concave 
surface, but only where the epithelium is in contact with the den- 
tal papilla. In the neck the cells become irregular in form. 
Over the convex surface the cells become lower and cuboidal. 
They ultimately atrophy and flatten out. The cells in the center 
of the enamel organs undergo a peculiar metamorphosis. They 
remain united together by a few thread-like processes. 

It is obvious from these changes in the embryo how what 
Robin calls the epithelial debris is derived from the epithelial 
cord, the follicular wall and the round bodies of lamina epithel- 
ium debris. According to Ch. Robin and Magitot,' who were 
the first to describe these • bodies, "The phenomena of budding 
commences, namely, when the epithelial cord has finished its 
course, having conducted the primary enamel organ to that point 
whence its subsequent evolution will be effected and soon after 
the formation of the secondary follicle, immediately after the 
rupture of the cord of the primitive follicle." Robin leans to 

'See their Memoir on the Genesis and Development of the Dental Follicle in 
Jour, de Physiologic de Brown-Sequard, 1860. 



the opinion that these bodies disappear soon after they are 
formed, " The time of their disappearance varies, they remark, 
in different species of animals. In the human embryo the 
remains of the cord of the primitive follicles may be found, even 
after the formation of the follicles of the permanent teeth, and 
it is probably during the process of eruption that these bud- 
dings become atrophied ; in the canine embryo the facts are 
nearly the same ; in the bovine and ovine embryos (calf and 
lamb) it has seemed to us that these proliferations disappear at a 


Fig. 24. — Section through the Incisive Portion of the Lower Jaw of an Ovine 
Embryo, Measuring 82 Millim (3J Inches) in Length. Magnified 260 Diam., 
after Drs. Ch. Legros and E. Magitot. 

D, Oral Epithelium. C, Lowest Layer of Cells in the Stratum Malpighii. 
F, Epithelial Cord. K, Bourgeon of the Secondary Cord. I, Follicular Wall. 
H, Dental Bulb. 

correspondingly earlier stage ; and we think it safe to say that, 
as a general rule, the complete absorption occurs toward the 
j>eriod of eruption." 

The embryology of the dental shelf, which has been sum- 
marized by Minot from Waldeyer, Kolliker, Von Ebner 1 and 
O. Hertwig, indicates the source of the structures which have 
been mistaken by Black for the limiting walls of glands. 

1 Handbuch der Zahnheilkunde, 1890, pages 209-262. 


After the epithelial cords of the temporary and permanent 
sets of teeth have been demarcated from their follicles, the proc- 
ess of cell building proceeds like the process of cord building. 
These buds, according to diaries Robin and Magitot, 1 are given 
off at the upper border of the follicle and below the epithelium 
of the gum. "In fact, as soon as the epithelial lamina loses its 
connection with the follicle, by the rupture of the cord, the epi- 
thelial cells composing it become greatly increased in number at 
the severed point. The multiplication of cell-elements results 



Fig. 25. — Vertical Transverse Section through the Incisive Region of the 
Lower .Iaw of Human Fostcs Measuring 38 Centimetres (15} Inches), Mag- 
nified SO Diam., after Drs. Cii. Legros and E. Magitot. 

b, Bony Formation. d, Oral Epithelium. g, Enamel Organs. H, Dental 
Bulb. I, Cord of the Permanent Follicle. K, Debris on the Follicular Wall of the 
Primitive Follicle and from its Cord. K, Epithelial Globule. L, Enamel Organ of 
the Permanent Tooth. 

in the formation of irregular buddings, which wander in different 
directions into the deeper portions of the embryonal tissue. 
These buddings vary greatly in form ; sometimes they are sim- 
ple cylinders, retaining their connection with the primitive 
lamina by pedicles of various lengths, and sometimes this slight 
connective is absorbed, thus isolating an epithelial mass." 

This budding occurs at different points along the cord (Fig. 
24 ) at the end and upon the outer surface of the follicular wall 
(Figs. 25 and 26) at the point where the cord is severed from the 

^oc. cit, 1S60. 


enamel organ. These gradually diminish as they descend upon 
its sides. Doubtless the epithelial cord remains in the periosteal 
and submucous tissue throughout life. Fig. 27 represents evident 
sections of epithelial cord in a man sixty-eight years of age, and 
Fig. 28 in a dog eight years. In the photographs of the scurvy 
cases and of dogs will be seen evidences of the persistence of 
epithelial debris late in life. The position already cited from 

'■'■';',' ■ ■-■ ■ * ■■■-■ 

'■ ■.' '' ."rtC'iTfiTuiroi- f) -,..„ ;.„,,,„ .-- : "' 


Fig. 26. — From the Lower Jaw of ax Ovine Embryo, Magnified 80 Diameters, 
Showing the Completed Dental Follicle and the Surrounding Tissues, 
after Drs. Ch. Legros and E. Magitot. 

a, Meckel's Cartilage. b, Traces of Ossification, c, Lowest Layer of Epithelial 
Cells, d, Oral Epithelium. F, Ameloblastic Layer. F, (Lower) External Layer of 
the Enamel Organ — a continuation of the Layer of Ameloblasts. g, Stellate reticu- 
lum of the Enamel Organ. H, Bulb. I, Follicular Wall. K, Buddings from the 

Robin and Magitot as to its early disappearance would hence 
appear to be too strongly taken. 

Robin and Magitot claim that this budding process occurs at 
or about the time of the rupture of the cord. Up to this period 
ossification has not taken place, but then deposits of bone appear 
in the fibrous tissue of the middle and outer surfaces. The bone 
deposit gradually takes the form of the jaw, filling in and 
encroaching upon the fibrous tissue, forming a bony wall on the 



one hand, and the crown and root of the tooth on the other. 
When the tooth is ready to erupt, the crown pushes the soft tissue 
laterally, while the root develops, forms a defined wall with the 
peridental membrane between them. The epithelial debris ( to 
use their term ) which before was scattered over the entire surface 
of the dental follicle, is now crowded into the very narrow space 

X 50. One-half-in. obj. No, Oc. 

Fig. 27.— Cross Section of Epithelial Cokd. Max. 

I, Peridental Membrane. W, Epithelial Debris or Cord. EC), Endarteritis Obliterans. 

of the peridental membrane, and owing to the position of the 
debris at the upper part of the follicle, it would be natural to find 
most of it at the peridental membrane. 


Development of the alveolar process is relegated to a series 
of cells situated in the fibers of the peridental membrane or 
fibrous tissne, and close to the margin of the bone tissue, and 



throughout the Haversian canals. These cells are called the 
osteoblasts. They perform the function of building up the bone 
tissue. Even after the alveolar process has developed its normal 
shape, so unstable is the nervous system which presides over 
these cells at this locality, that at the slightest provocation, either 

X 560. No. 2 projection ocular. One-twelfth obj. Zeiss. 

Fig. 28. — Cross Section Epithelial Cord. Doo. 

I, Peridental Membrane. W, Epithelial Debris or Cord. U, Nerve Tissue. 

local or constitutional, they will continue their process of con- 
struction. Hence, the frequency of hyrjertrophy of the j^rocess, 
and in disease the calcification of the peridental membrane. 

On the other side of the membrane, next the root surfaces, 


may be seen other ceils which build up and destroy the cemen- 
tum; these arc called cementoblasts and cementoclasts. These 
arc of little importance in this connection with the study of this 
disease, although they are frequently present and at work when 
inflammation of the membrane occurs. 

There is, however, another class of cells found in the peri- 
dental membrane of the utmost importance in this connection, 
the osteoclasts, located in the fibers, and in close proximity to 
the alveolar wall, and around the inner border of the Haversian 
canals. The function of these cells is to tear down irregular 
bone and tooth structure due to unstable nervous tissue, and from 
the slightest irritation. 

The gums, mucous membrane, alveolar process and peridental 
membrane, owing to their transient nature, are influenced by the 
slightest irritation. This influence is the result of both constitu- 
tional and local causes. It consists of an irritation in the periph- 
eral nerves which sets the osteoblasts and osteoclasts at work 
to build up or tear down the alveolar process. This influence 
may be only sufficient to stimulate these cells to action without 
inflammation. This is noticed in the advance toward old age in 
long, lingering debility, in the development of bone, especially 
the tearing down and the building up of the inferior maxillary 
backward. It may be noted in mild or intense inflammation of 
the peridental membrane, due to more acute forms of disease, to 
scurvy, mercurial, lead and iodide poisoning, or to local irrita- 
tion. So sensitive are these structures that in neurotics and 
degenerates the slightest irritation produced in the physiologic 
development of the permanent teeth is sufficient to start the 
osteoblasts to building up bone structure, thus producing that 
pathologic condition called hypertrophy of the alveolar process; 
one of the most marked evidences of an unstable nervous 

The breaking down of the tissues by the osteoclasts may be 
induced by as slight a cause. The alveolar process being so thin 
about the teeth, destruction of the entire walls is accomplished 
without difficulty, and in a very short time, thus loosening the 
teeth, which eventually drop out. 

According to Kaufmann 1 the following processes take part in 

1 Pathologische Anatomie. 



the absorption of bone: (a) Lacunar Absorption, (b) Forma- 
tion of Perforating Canals, (c) Disappearance after Prior 
Absorption of Lime (Halisteresis) (Bony Waste) and Osteo- 

"By far the commonest form of bone destruction is by lacunar 
absorption. This process occurs not only under physiologic 
conditions, but is extraordinarily frequent in pathologic states, 
e. g., in the various types of atrophy. They form on the 
smooth, superficial surfaces of the bone deep grooves (so-called 
Howship's lacunas) in which lie smaller or greater polynuclear 
cells (osteoclasts, Kolliker) which evidently blend together (Fig. 
29). There are no alterations of the bone substance that would 

Fig. 29. 

a, Bone Trabecular b, Tubercle with Granulation Tissue, e, Broken-down Tissue. 
d, Blood Vessel, e, Osteoclasts. /, Fat Cells. 

indicate a primary line of absorption (Plummer). The con- 
fluence of these lacunae form larger cavities. 

" The second form of bone absorption, which is occasionally 
met under physiologic conditions, is by means of perforating 
canals (so-called Volkmann canals). Under physiologic condi- 
tions canals occur in varying numbers in the lamella? (general 
lamella?) which contain vessels (perforating vessels). These are 
often associated with the Haversian canals and gradually pass 


into them, but unlike them, are surrounded with circular lam- 
ellae. Under pathologic conditions the conception of these per- 
forating canals is somewhat widened. On the one band 
Volkmann's canals are spoken of when reference is made to the 



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Fig. 30. 

a, Large Spaces Resulting from Absorption of the Trabecule. b, Decalcified Bone, 
c and d, Decalcified Bone and Atrophied Trabecule. e, Haversian Canals. 

vessels or vascular connective tissue penetrating from one medul- 
lary space in the spongy substance, or from one Haversian canal 
in the compact substance, to another, in such ;i way that ;i passage 
i.s made from one part of the hone to the other; Volkmann's 
canals also include irregular ampula-formed dilations or cavities 


(Fig. 30). By confluence of these are produced cavities or irreg- 
ularly outlined canals penetrating the bone substance. These, if 
they empty into the medullary space, become filled with cells. 

" Under much rarer conditions, especially in senile marasmic 
osteomalacia and also in that occurring in pregnancy, bone 
absorption takes place after a prior abstraction of lime (halister- 
esis) and the remaining substance (bone cartilage) is then further 
dissolved, passing through a temporary fibroid stage. This 
destruction of the decalcified and interfibrillse decomposed bone 
is produced as a rule without osteoclasts. The decalcified border 
zones of the trabecular appear with simple carmine (coloring) or 
by double stains." 



The etiology of interstitial gingivitis, according to the views 
summarized previously, is divisible into local and constitutional. 
While one school leans largely to the local etiology, another 
advocates as strongly the constitutional theory. In a general 
way. etiology may he divided into exciting and predisposing. 
Etiology may also depend upon an element dependent on the 
exciting cause, an element dependent on the constitution of the 
individual attacked, and finally an element dependent on his 
condition when attacked, both as regards his general system 
or any one of his organs. The chief constitutional causes to 
which the disease has been ascribed are general conditions of the 
health, heredity, constitutional disorders, excessive lime salt 
secretion, meat-eating, nervous exhaustion, scorbutus and uric 
acid states, as well as environment. The local causes assigned 
are acute inflammation of the mucous membranes, catarrhal 
states, germs or fungi, irregular teeth, lactic acid, pocket dis- 
ease, hemorrhagic deposits, seminal calculi and uncleanliness. 
That all these factors exercise an influence is undeniable, but 
the enormous etiologic role which has been assigned to some of 
them is the result of generalization from too few cases. Many 
of the assigned causes could lie compressed into fewer etiologic 
influences. Thus meat-eating and the uric acid states are too 
intimately connected to be regarded as different causes, from a 
constitutional standpoint. As has been already pointed out, uric- 
acid acts, when it acts at all. like lactic and other acids, as a local 
irritant rather than as the constitutional condition (as many -ii|i- 
pose) which underlies its production and of which it serves as an 

Scorbutus is an expression of a nutritional disorder due very 
frequently in the adult to an excess of meat or a monotony of 
diet. It is a constitutional disorder, peculiarly apt to have its 
local expression in the gums long ere the general constitutional 


symptoms are manifest. The germs and fungi etiologists, on the 
other hand, tend to ignore the constitutional state behind the 
local culture medium, which must be furnished before growth of 
the germ or fungus can occur. In order, therefore, to determine 
whether an alleged cause be exciting or predisposing and what 
is the influence of the etiologic moment, as the union at one time 
of the two constitutional factors already cited is called, analysis 
is required of all the varied factors charged with producing the 
disease. The influence of heredity is generally left out of con- 
sideration unless it be direct, which it rarely is, since heredity, 
as has been well remarked, is usually a prophecy rather than a 
destiny. It hence constitutes, as a rule, a predisposition. 

The chief tissues concerned in the elimination of waste prod- 
ucts are the skin, the lungs and air passages, including the 
mouth and nose, the kidneys, liver and intestines. Interference 
with the eliminatory powers of the kidneys, liver and intestines 
is especially apt to throw extra work on the skin, lungs and air 
passages. Of this a sour-winey odor of the breath in diabetes is 
an excellent illustration. What is true of such a marked form 
of suboxidation, resulting in auto-intoxication, is true of less 
pronounced forms. The peculiarly foul odor of the breath and 
skin in fsecal intoxication indicates that the mucous membranes 
of the nose, throat, mouth and gums are doing the work of 
elimination which should have been done by the intestines. 
The failure of the kidney to perform its share of eliminatory 
work is most apt, however, to find expression in the skin, lungs, 
nose, mouth and gums. 

The influence of the nervous system on the growth and 
repair of any tissue is admitted by every physiologist. This 
influence is entitled the trophic function of nerves. It is not, 
however, exactly settled whether it be exerted through the 
nerves themselves or secondarily through their control of the 
vaso-motor (blood vessel) system. Many trophic disturbances, 
as J. Collins 1 remarks, are probably due to vaso-motor changes, 
and it is not possible to separate by any sharply defined line the 
vaso-motor from the tropho-neuroses. At the same time, it 
should be distinctly remembered that there exist tropho-neuroses 
in which there are no appreciable vaso-motor change as in many 

1 Nervous Diseases, by Dr. F. X. Dercum. 


cases of acromegaly and hypertrophies. On the other hand, 
there are any amount of vaso-motor disturbance which arc by 
no means trophic in character. Trophic disturbance, which may 
play a very important part at the onset of interstitial gingivitis, 
is neurotic oedema due to nerve irritation. While this is most 
frequent on the face, lips, tongue, pharynx, forehead and genital 
organs, it also appears on the gums. The oedema reaches its 
full development from one-half to two hours. There is a feeling 
of stiffness and unyieldingness, but no sensation of inflammatory 
swelling. This type of trophic disorder often initiates changes 
in the mucous membrane which may readily form the basis of 
interstitial gingivitis. This condition may not be only due to 
ordinary nervous causes, but may arise from constitutional con- 
ditions, gout, etc., and toxic influences. 



AVhat John Fitzgerald 1 calls the gingival organs, possess, as 
he remarks, in common with some other tissues of the body, the 
power of selecting and excreting poisonous substances from the 
blood. Some of these cause hyperemia, or even inflammation, in 
their passage. Uric acid has been found to play a part in so- 
many excretions that it has naturally attracted attention here. 
The trend of medical opinion has set strongly in this direction, 
but of late this trend is changing. 

During the past two decades uric acid has assumed again the 
prominence in pathogeny which it once had when called sup- 
pressed gout. It is not surprising, therefore, to find that Reeves, 
Pierce, Kirk, Rhein and others claim a uric acid etiology for 
interstitial gingivitis. In support of this claim are advanced the 
results of three experiments which Pierce has had made on 
tooth deposits. These deposits were examined chemically by 
Ernst Congdon, of the Drexel Institute. 2 The first specimen 
contained a number of needle crystals of calcium urate, a few 
crystals of free uric acid and crystals of calcium phosphate. 
Destructive distillation gave a strong amnionic reaction. The 
murexid test for uric acid and its compounds gave faint results, 
although its characteristic color was evident in several places. 
The second specimen presented the same crystals. The reaction 
to the murexid test was strong and resulted in a number of 
purplish-red spots. Similar results were obtained from the third 
specimen. A. B. Brubaker examined six or eight specimens 
in Pierce's presence, with like results to those obtained in the 
previous examination. In three an abundance of sodium urate 
crystals was present. 

The great deficiency in the experiments thus described is the 
small number of cases examined and the lack of jDroper control 

1 The Clinical Journal, March 1, 1899. 

2 International Dental Journal, Vol. XV, pages 1, 217, 501. 


experiments. These elements have so frequently led to errors in 
dental pathology that I determined upon a series of investigations 
in two different laboratories, whose results were reported some 
years ago. 1 The Columbus Medical Laboratory was selected for 
one series of experiments in special cases. The laboratory of the 
Northwestern University Woman's Medical School was selected 
for the other series of experiments, to which teeth were sent as 
soon as they were obtained. One hundred and fifteen teeth were 
sent to the laboratory last named from three institutions in 
Chicago which make a specialty of extraction. These teeth had 
no history other than the fact that the cases were well-marked 
instances of interstitial gingivitis with plenty of calcic deposits, 
and that the teeth were loose in the sockets when extracted. ( )f 
the one hundred examinations made in the Columbus Medical 
Laboratory, fifty were upon specimens of calcic deposits from my 
patients and fifty were upon specimens obtained from the institu- 
tions just mentioned, and were therefore without history. The 
tests employe! 1 were the hydrochloric acid, the dry distillation, 
and the murexid, these being the tests recommended by Pierce. 
The examinations in the Columbus Medical Laboratory were 
made by J. A. Wesener, and those in the laboratory of the 
Northwestern University Women's Medical School by J. H. 

Of the one hundred and fifteen examinations made at the 
Northwestern University Woman's Medical School by the first 
test, in only two case- was found the needle-shaped crystals, and 
one in which there was a slight resemblance of uric-acid crystals. 
By the dry distillation test, thirteen gave no reaction from 
ammonia, and in seven the reaction was slight. The remaining 
eighty gave a decided reaction. By the murexid test, four gave 
a slight murexid color, hut remainder gave no reaction. Special 
examination was made of twelve of these teeth by the addition 
of strong hydrochloric acid, warming, decanting the acid, and 
washing with water. These gave no reaction by the dry distilla- 
tion tests for ammonia. Two gave a slight reaction by the 
murexid test. In examination of the teeth of three uric-acid 
diathetic women, over forty years of age, uric acid was not 

1 Dental Cosmos, April, 189(5, page 310. Journal of the American Medical Asso- 
ciation, January 16, 1897. 


detectible either by the murexicl test or microscopically. The 
examinations made in the Columbus Medical Laboratory were 
still more interesting, since among them were specimens from 
patients whose history could be obtained. Of the fifty obtained 
outside, eight gave positive results from all three tests. The 
other forty-two were positive by dry distillation, and negative by 
the murexid and microscopical tests. Of the fifty patients, 
thirty-eight females and twelve males, thirty-two were over forty 
years of age, twelve over thirty years, and six over fifteen years. 

Twenty-six have uric acid to a greater or less extent, nine 
suffer with indigestion, seven of which are subject to sick head- 
ache, thirty-four have rheumatism. Six are English, and four of 
these have the true gout ; the other two have rheumatism. 

All are positive with the dry distillation test, All are nega- 
tive with the murexid test. Forty-nine are negative with the 
microscopical test, One shows needle-shaped crystals, but not 
uric acid. It is a singular fact that in both laboratories, the 
cases in which there was uric acid and gouty histories gave nega- 
tive results. By the dry distillation test, out of two hundred 
and fifteen cases, all but twelve cases (which have been treated 
to remove nitrogenous material) responded. The twelve cases so 
treated did not respond, since nitrogenous compounds in and 
about teeth (even the saliva) burned to an ash will produce 
ammonia. By the murexid test only twelve out of the two 
hundred and fifteen gave a jDositive reaction. By the micro- 
scopic examination but ten showed crystals. One of the chemists 
who made the examination is positive that they were uric acid 
crystals. The other is not, since lime-phosphate crystals resemble 
uric acid crystals too minutely to be distinguished positively. 

For three years Wesener made further examinations as to the 
relative value of the three tests employed. According to his 
experiments the murexid test is the most valuable, the crystal 
test second, and the dry distillation third. The murexid test is 
the most reliable in testing tartar for uric acid, since its red color 
is easily distinguished from other colors and the test is simple in 
application. The test for crystallized uric acid is very unsatis- 
factory, since here must be dealt with a complex mass which not 
only contains crystals of calcium phosphate (very similar to those 
of uric acid) but a great mass of detritus obscuring the crystals 


of uric acid. If crystals be present the)' by no means settle the 
existence of uric acid. When the faintest quantity possible of 
uric acid is mixed with tartar from teetb and subjected to crystal- 
lization, the results are always negative. If subjected to the 
murexid test, the results are always positive. The dry distilla- 
tion test is so inaccurate as to be unworthy consideration. 

Since these results were published, seven hundred and thirty- 
five cases have been examined. These examinations were con- 
ducted by Jerome H. Salisbury, now of Rush Medical College. 
The teeth procured from institutions which make a specialty of 
extracting contained the dark calcic deposit above the pus line. 
By the murexid test, six out of the three hundred gave a distinct 
reaction ; eighteen showed crystals under the microscope. The 
murexid test was performed as follows: The deposit was selected 
as carefully as possible, removed from the tooth, and placed in a 
small porcelain crucible. A drop of pure nitric acid was added 
and the mixture evaporated on the water bath. When dry, the 
evaporation was repeated with another drop of nitric acid, and 
the crucible allowed to cool. When cool, the color produced by 
the nitric acid was observed, and then a glass rod, wet with 
ammonia water, was brought near the deposit, and any color pro- 
duced was noted. If no color was observed, the ammonia was 
allowed to flow over the residue. A yellow color was produced 
in many cases by the nitric acid, which was deepened by the 
addition of ammonia. The microscopic examination was made 
by scraping off the deposit and evaporating it with a drop of 
hydrochloric acid. The residue was moistened with water, and 
the insoluble material placed on a slide and covered with a 
cover-glass. It was examined with a No. 7 objective. Uric 
acid, therefore, occurred in a certain very small proportion of 
cases of calcic deposit on the teeth. 

Four hundred and thirty-five cases were later examined, mak- 
ing in all nine hundred and fifty. Out of these four hundred 
and thirty-five cases only four per cent showed uric acid by the 
murexid test and eight per cent by the crystal test. Since the 
crystal test is not so accurate as the murexid test, it is safe to say 
that six per cent was the actual pel- cent of uric acid. A- a 
result of the different experiments, in the first two hundred and 
fifteen cases five per cent uric acid was found. In the second 


three hundred cases, four per cent, and in the third four hundred 
and thirty-five cases, six per cent was found. In an examination 
of nine hundred and fifty cases by different chemists at different 
periods, five to six per cent give positive results as to uric acid by 
the chemic and microscopic examination. These results demon- 
strate conclusively that interstitial gingivitis is not due solely to 
uric acid ; that uric acid when found is merely an expression of 
the uric acid diathesis and a coincidence, since it is not always 
present in the gums and tartar of patients attacked either by gout 
or the uric acid diathesis. In the six per cent of cases there was 
nothing to show that uric acid was the cause of interstitial gingi- 
vitis, since the deposits were examined after the teeth had been 
removed. Any other irritation may have been the exciting- 
cause. Uric acid acts, when at all, solely as a local irritant. 



The foods which enable the body to repair its waste, to build 
up new tissue and to supply the energy, arc divisible into four 
classes: the inorganic substances, the fats or hydrocarbons, 
and the starches and sugars, or carbohydrates, and the proteid 
compounds. These divisions are, however, relative, since the 
proteids may contain both hydrocarbons and carbohydrates. 
The inorganic substances, such as water, phosphates, chlorides, 
carbonates, sulphates, etc., enter the body, as a rule, under their 
own form, either alone or in combination with other classes. 
They are not oxidized or split up within the system to enter into 
the chemical formations of other compounds, but are united 
mechanically with the proteid group. These bodies act, as a rule, 
in a purely mechanical manner. After having served their pur- 
pose, they pass out of the system with the excretions, compara- 
tively unchanged in their composition. They are the only 
mem her of the group of foods which are of a special interest in 
the present research. The inorganic salts have, however, not 
received the attention from physiologic chemists that their 
importance demands. They are, as a rule, found in greater or 
lesser quantity in all foods that are taken into the body. They 
do not serve as a source of energy, but as the other foods are 
needed for the development of the tissues, so the inorganic salts 
are needed for the building of bone tissue and the repair of 

waste. This is accomplished by the soluble salts in the 1>I I. 

Human blood has the following composition : 


Max. Woman. 

25 Years. 30 Years. 

Water 788. 71 824. 55 

Solids 211.29 .... 175.45 

Proteids and Extractives 191.78 .... 157.93 

Fibrin 3.93 1.91 

Htematin (and iron) 7. 70 .... 6. 99 

Salts ' 7.88 .... 8.62 



CI .. 










CI . .. 





NA 20 

NA 20 . 






M t „, . 

■P'205 • • 

CaO . 

M qn . . . 


These acids and bases exist, of course, in the plasma and the 
corpuscles as salts. It is not possible to determine exactly how 
they are combined as salts, but Schmidt suggests the following 
combination : 


Potassium Sulphate 0. 132 

Potassium Chloride 3. 679 

Potassium Phosphate 2. 343 

Sodium Phosphate 0. 633 

Sodium Carbonate 0. 341 

Calcium Phosphate 0. 094 

Magnesium Phosphate 0. 060 


Potassium Sulphate 0:281 

Potassium Chloride 0.359 

Sodium Chloride 5. 546 

Sodium Phosphate 0. 271 

Sodium Carbonate 1. 532 

Calcium Phosphate 0.298 

Magnesium Phosphate 0.218 

It will be seen that the corpuscle contains an excess of 
potassium salts, and the plasma contains an excess of sodium 
salts. All parts of the blood contain salts, however. 

Throughout the entire body, there is a rich supply of blood 
vessels penetrating every tissue. The plasma of the blood pass- 
ing by exosmosis through the walls of the capillaries is thus 
brought in immediate contact with the tissues to which it brings 
nourishment and oxygen of the blood, and from which it 
removes the waste products of metabolism. Other usable prod- 
ucts or lymph are collected in small capillary spaces, which in 
turn open into definite lymphatic vessels. These vessels unite 


into larger and larger one*, which eventually pour this usable 
waste product into the great thoracic or left lymphatic ducts, and 
a second smaller right lymphatic duet. These in turn empty 
into blood vessels, each upon its own side. The lymph contains 
essentially the same constituents as the blood plasma, and the 
salts are found in the same proportion as in it. They are then 
eliminated through the sweat glands, tonsils, mucous glands, 
kidneys, large intestines and salivary glands. 

The composition of the deposits in the various parts of the 
body vary according to the locality and the character of the 
excreta eliminated in connection with them. 

The chemical composition of the human bile, according to 
Jacobson, 1 is as follows : 

Water 977 . 40 

Sodium Glycocholate 9 . 94 

Cholesterin 0.54 

Free fat . 10 

Sodium palmitate and sterrate 1 . 26 

Lecitine a . 04 

Other organic matter 2 . 2t> 

Sodium chloride 5 . 45 

Potassium chloride 0.28 

Sodium phosphate 1 . 33 

Lime phosphate 0.37 

Sodium carbonate . 93 

Of this analysis the solid ingredients constitute 22.5 parts per 
thousand, of which two-thirds are organic and one-third inor- 
ganic. The inorganic salts of the bile are in most cases returned 
to the blood, where they are redistributed to the tissues. Occa- 
sionally, however, gall stones occur, which are composed of 
(analysis H. I). Geddings 2 ): 

Moisture 3 . 32 

Biliary matter 32 . 182 

Cholesterin 54 . 952 

Matter soluble in ether 7.77 

Iron traces 

Phosphoric acid traces 

Lime traces 

Magnesium traces 

1 American System of Dentistry. 

2 Transactions 8outh Carolina Medical Association, 1SS0. 


Secretions of the pancreatic juice (dog) by C. Schmidt are as 
follows : 

Water 900 . 76 

Solids 99 . 24 

Organic substances 90 . 44 

Ash 8.80 

Sodium carbonate . 58 

Sodium chloride 7 . 35 

Calcium magnesium and sodium phosphate . 53 

The composition of the normal human pancreatic juice has 
not been determined completely owing to the difficulty of obtain- 
ing the secretion. According to Zawadsky the composition of 
the secretion of a young woman was as follows : 

Water in 1.000 parts 864.05 

Organic substance in 1,000 parts 132 . 51 

Proteids in 1, 000 parts 92 . 05 

Salts in 1, 000 parts 3 . 44 


" Of the inorganic salts, NaCl is by far the most abundant ; 
it occurs in quantities varying from 2 to 3.5 parts per thousand. 
The elements of the sweat which are of importance from an 
excretory standpoint are water, inorganic salts and urea or related 
nitrogenous compounds." 

Inorganic salts from the faeces are made up of the salts of 
sodium, potassium, calcium, magnesium and iron. According to 
Enderlin 1 the following represent the composition of the material 
matter in the faaces : 


Sodium chloride and sulphate 1 . 37 

Sodium phosphate 2 . 63 


Earth phosphate 80 . 37 

Ferric phosphate 2 . 09 

Calcium sulphate 4 . 53 

Silicic acid 7 . 94 

Like other constituents of the lymph, the salts vary consider- 
ably in proportion, according as the fluid is more or less rich in 

1 Gamgee, Physiological Chemistry of the Animal Body. 


water. The salts are much more abundant than the organic 

Inorganic salts in the urine consist, according to Howell, 1 
chiefly of chlorides, phosphates and sulphates of the alkalies and 
the alkaline earths. As a rule they arise partly from the salts 
ingested with the food, which salts are eliminated from the blood 
by the kidney in the water secretion, and in part they are formed 
in the destructive metabolism which takes place in the body, 
particularly that involving the proteids. Sodium chloride occurs 
in the largest quantities (about 15 grams per day), of which the 
greater part is derived directly from the salt taken in the food. 
The phosphates occur in combination with Ca and Mg, but chiefly 
as acid phosphates, of Na or K. The acid reaction of the urine 
is caused by these latter. The phosphates are produced in part 
from destruction of phosphorus-containing tissues in the body, 
but chiefly proceed from phosphates in the food. Following are 
the average quantities in grams of the chief substances normally 
excreted in the urine in six hours r 

Water 1440 — 1500 

Solids 57 — 68 

Organic : 

Urea 28 — 68 

Uric acid 7 

Hippurie acid 3 — 2 

Kreatiniu 1.7 — 2.1 

Inorganic : 

Sodium chloride 15 — 20 

Phosphoric acid 2.5 — 3 

Sulphuric acid 2 — 2.5 

Sodium 5 — 7 

Magnesium .04 

Potassium 3 — 4 

Calcium .03 

Urinary calculi (classified according to their principal ingre- 
dients), are divided into : 

1. Uric stone, composed of uric acid and acid urates. 

2. Oxalic stone, composed of lime oxalate. 

3. Phosphoric stone, which are composed of magnesium phos- 
phate and carbonate with urate of ammonia. 

1 American Text-Book of Physiology. 

2 Landolt, Physiology. 


Each one of these compounds is nearly in a pure state. A 
stone may be composed entirely of one salt or it may be composed 
of two, three or four, each compound forming separate consecu- 
tive layers through the stone. One examination made by How- 
ship Dickinson 1 showed eighty-nine per cent lime carbonate and 
the rest lime oxalate and phosphate of lime. 

The deposits upon the teeth are derived partly from the salts 
ingested with foods, which salts are eliminated from the blood in 
water secretion, and in part they are found in the waste of tissue 
which takes place in the body. 

The saliva, according to Schmidt, is made up of the following : 

Water 991 . 45 

Organic material 2 . 89 

Inorganic : 

Calcic chloride 4.50 

Sodium chloride .... 

Calcic phosphate 1.16 

Magnesium .... 


This material floating in the saliva, together with the epithe- 
lial scales and other extraneous matters, contribute to form what 
is known as tartar. This material collects upon the teeth, and 
according to examinations by Stevenson consists of: 

Soft tartar Hard tartar 

on molars. on lower incisors. 

Water and organic matter 21 . 48 .... 17 . 51 

Magnesium phosphate 1.31 .... 1.31 

Calcium phosphate with a little car- 
bonate and trace of fluorine .... 77 . 21 .... 81 . 18 

100.00 .... 100.00 

Another analysis made by Scheheoetskey resulted thus : 

Water and organic matter 22. 07 

Magnesium phosphate 1 07 

Calcium phosphate 67.18 

Calcium carbonate 8.13 

Calcium fluoride 1.55 

1 Renal and Urinary Affections. 


Malenfant found that salivary calculi (located in Wharton's 

duct) was composed of: 

Lime phosphate 27 

Magnesium phosphate 1 

Basic lime phosphate 60 

Alcohol and muriatic acid 4 

Ptyalin 2 

Loss 6 

The following are results of analysis of salivary calculi by 
various observers : 


100 Parts. 






2 3 


Calcium carbonate. . . 



80 . 7 





Calcium phosphate . . . 








Magnesium phosphate 



Soluble solids 

Organic matter 



8.3 j 





Water and loss 


2.3 1.7 


Deposits in the tissues in gout are made up of soda and lime 
urates. In order to compare the calcic deposits in other parts of 
the body with the serumal deposits upon the teeth affected with 
interstitial gingivitis, thousands of teeth were obtained from three 
dental offices which make a practice of extracting teeth. From 
these one thousand were selected at two different times, making- 
two thousand teeth containing deposits direct from the tissues. 
These were submitted to a chemical analysis by J. H. Salis- 
bury, at Rush Medical College, who reports as follows : 

" The method which I employed in analysis of calcic deposits 
was as follows : The material was so selected as to be free as 
possible from salivary tartar and a weighed portion was dried at 
100° C. This was then carefully incinerated and again weighed, 
and the difference calculated as organic matter. The residue 
after incineration was divided into two portions, A and B. 

"A was used for the estimation of phosphates as follows : 
The ash was dissolved in nitric acid and the solution precipitated 
with ammonium molybdate. The precipitate was washed, dis- 
solved in ammonia precipitated by magnesia mixture and the 


precipitate of ammonia magnesium phosphate, washed, dried, 
ignited and weighed. 

" In B, calcium and magnesium were estimated as follows : 
The ash was dissolved in hydrochloric acid and the acid just 
neutralized with ammonia water and sodium acetate added. It 
was then made slightly acid with a drop of hydrochloric acid 
and precipitated with ammonium oxalate. The precipitate of 
calcium oxalate was filtered off, washed, converted into calcium 
oxide and weighed. The nitrate was made alkaline, sodium 
phosphate added, and the precipitate of magnesium-ammonium 
phosphate collected, washed, dried, ignited and weighed. In 
case the phosphoric acid determined in A did not saturate the 
calcium and magnesium obtained in B, the excess of base was 
calculated as carbonate. 

" The following is the composition of the serumal tartar 
according to analysis of April 18, 1898 : 

Water and organic matter 32 . 24 

Magnesium phosphate 98 

Calcium phosphate 63 . 08 

Calcium carbonate 3.70 


"Analysis of the serumal tartar, October 24, 1898, shows it to 
have the following composition : 

Water 4.48 

Organic matter 27 . 00 

Calcium phosphate 72 . 73 

Magnesium phosphate 4. 91 


While nearly every kind of food taken into the stomach con- 
tains inorganic salts, every excretory organ of the body throws 
out a certain amount of these salts. Some of these organs 
excrete the salts in a pure state, while in others the salts are 
combined with acids or fluids peculiar to that organ. These salts 
differ in composition and quantity on different days, at different 
hours of the same day ; differ at different ages of the same person 
and differ in persons of like age, on the same diet. No matter 
how careful the chemist may be in analysis, no two results will 
be exactly alike. For this reason, in tartar and calcic deposit 


upon the roots of teeth, two different analyses of the same deposits 
are cited. It is evident that while slight differences occur in the 
table, these are due chiefly to the character of the secretions. 
The kidneys and salivary glands clearly excrete most of the waste 
inorganic salts. 

Since each excretory organ has its part in elimination of 
waste inorganic salts, it is clear that if one organ becomes tired 
or diseased, other organs have an extra amount of material to 
excrete. In any event, the blood becomes surcharged with waste 
inorganic salts. There is a class of patients with deformed jaws 
and irregular teeth, tonsil hypertrophy, mucous membrane, 
nasal bone and post-nasal space disorder, adenoids, arrest of the 
facial bones. They are neurotics and degenerates. This class 
comprehends those whose nervous system is unstable and whose 
physical development is a departure from the race type. This 
unstable or tired condition may affect but one excretory organ. 
In most cases it affects all organs as well as the entire body. In 
these patients, especially in youth, does hypertrophy of the alve- 
olar process take place and large deposits are observed upon the 
teeth. In this class may be placed rachitic children. 

Inorganic salts taken in food are generally utilized until the 
osseous system has attained its growth. This usually occurs at 
about the twenty-sixth year, but full growth may not be attained 
until the thirty-sixth year. When this period has been reached, 
although the body still has the same supply of inorganic salts, 
the system can assimilate only what it needs. The remainder 
becomes waste. Under such conditions the blood is overcharged 
with these salts. 

A condition of the system, which has received too little atten- 
tion, occurs in a class of children ranging from six to eight 
years, who excrete larger quantities of inorganic salts through 
the kidneys and salivary glands. In such cases the teeth 
become coated with tartar. The gums become inflamed from 
irritation. Interstitial gingivitis is developed in youth. These 
children may be rachitic, or border upon the disease. They are 
neurotic, degenerate, suffer from rachitis, rapid decay of the teeth 
and irregularities. They occur in American and European 
schools of idiocy and for dependent and defective children. 
From seventy-five to ninety per cent of these children have 


interstitial gingivitis, ranging from simple inflammation of tli e 
gums to absorption of the gums and alveolar process with pus 
exudate. Miller noticed in an examination of twenty-six cases 
of rachitic children under twelve years of age that seven mani- 
fested pronounced symptoms of interstitial gingivitis. This was 
no doubt due to accumulation of calcic salts upon the teeth, 
producing irritation and absorption of the alveolar process and 
contraction of the gums. 

In cases where large collections of tartar are deposited upon 
the teeth of children there is also an excess of excreta through 
the kidneys. Examination of urine in such cases will reveal 
always from four to eight times more deposit than the normal 
for the age of the patient. Defective nutrition is the result, the 
bones are small, and the jaws and teeth are irregular. The teeth 
decay early in life and it is with difficulty that the decay can be 
arrested. What is true of children is also true of people at 
advanced age. 

'After the skeleton had attained its growth (even in those 
cases where no deposits were before observed) the blood became 
overcharged with lime salts and the teeth became a nidus for the 
deposit from the salivary glands. It is, therefore, clear why 
deposits and inflammation of the gums are so common after the 
twenty-sixth year, and more common later in life. Defective 
children and people who have obtained their growth are more 
susceptible to trophic disorders of nutrition and the tissues take 
on disease more readily than healthy individuals earlier in life. 
When inflammation takes place in connective tissue in all parts 
of the body (especially if the blood be surcharged with inorganic 
salts) deposits take place in that tissue through the capillary 
system. On the other hand, when inflammation of the connective 
tissue takes place, if inorganic salts be scarce in the blood, 
deposits do not take place. As is elsewhere shown, 1 calcic 
deposits on the roots of teeth are a result of inflammation and 
pus infection and not the cause. 

1 International Dental Journal, April, 1S96. 



The influence of heredity in interstitial gingivitis, as in other 
morbid conditions, is still a mooted question. Morbid heredity, 
as I have elsewhere shown, 1 is practically divisible into direct and 
indirect. In the first type the morbid condition is directly inher- 
ited ; in the second, a deficiency is due to the morbid condition 
which may or may not express itself in a tendency to the morbid 
condition of which it is the offshoot, Heredity further should he 
separated from congenital states which result from the operation 
of germs or toxins during a particular pregnancy wherein these 
pass through the placenta to the foetus. A child may he born of 
a tuberculous mother with a tendency to tuberculosis, but the 
tubercle bacili may also directly infect it through the placenta so 
that it is born with tuberculosis. The first is the inheritance of 
the weakened organism of the mother. The second is a condition 
of intra-uterine infection. 

The reported cases of direct heredity of the pyorrhoeic stage 
of interstitial gingivitis may afford instances of one or the other of 
these- categories. As has elsewhere been shown, transitory organs 
are peculiarly apt to lie weakened by heredity both in their 
structure and in their resistance to morbific germs and agencies. 
These weaknesses . are especially apt to he shown during the 
period of systemic stress connected with the first and second 
dentition. Such weaknesses may lie the outcome of general 
nerve exhaustion on the part of the parents (the mother espe- 
cially), and constitutes transformed heredity, which is far more 
frequent than direct. This transformed heredity may he more 
intense than the constitutional deficiency of the immediate 
ancestry. .On the other hand, the conservative influence of 
several generations may so offset the evil results of the defect- in 
the parents that the inheritance of defect is slight, if at all 

Degeneracy; Its Si<_rns. Causes and Effects 


This last tyr^e of heredity is called atavism (or "throw-back,"' 
by the breeders). It is more likely to work for good than evil, 
albeit the evil effects are more generally looked for. Because of 
this atavism a serious nervous defect in a parent might express 
itself only in an increased tendency to disease on the part of 
transitory structures. The periods of stress are times in the life 
of man when certain great life functions are developing or under- 
going retrogression. These periods of development or evolution 
are marked by the tw r o dentitions and the development of the 
sexual organs, which might more aptly be called the third den- 
tition, since ere its close the wisdom tooth appears, if at all. The 
periods of retrogression are when the great sexual functions are 
undergoing involution or when the whole body is undergoing 
senile change. These periods often constitute an etiologic 
moment for the production of disease even when potent heredi- 
tary defect is absent, albeit at these periods such defect is apt 
to appear. 

Another possibility to be considered in this connection as 
complicating the diagnosis of heredity in disease is environ- 
ment, understanding by this term all the external conditions that 
can favor the development of a disorder. Family habits and 
surroundings are apt to be alike for every member. If anything 
in the environment especially favors the breaking out of a disease 
in one member, the cause is equally apt to be effective with 
another, provided the individual idiosyncrasy is similar. This 
may give rise to a suspicion of heredity, since conditions of life, 
family habits and intimate household surroundings favor the 
occurrence of a disorder in several members or generations of the 
same family. Habits are often transmitted by imitation from 
parents to offspring. These may be direct exciting or predis- 
posing causes of an affection, especially if it be more or less 
favored by their existence. 

That constitutional 'conditions of hereditary origin favor the 
occurrence of interstitial gingivitis is undeniable, but this does 
not prove that gingivitis itself is hereditary. They favor its 
occurrence as they favor other morbid conditions, by lessening 
resistance, or by preparing the way. The gingivitis is only one 
of the many accidents that are thus facilitated. So far as sali- 
vary concretions are to be regarded as an exciting cause, heredity 


may be disregarded, since these (though varying widely in dif- 
ferent individuals in the amount of the deposit, and consequently 

the irritation produced) are dependent upon more remote con- 
stitutional or loeal conditions without direct connection with the 

The varieties (charged to lithaemia or arthritic conditions 
notoriously hereditary) are of accidental origin rather than essen- 
tially connected with constitutional conditions that happen to 
furnish the irritant. 

Local uric acid poisoning 1 is. as I have elsewhere shown, 
occasionally associated with gingivitis. The coexistence illus- 
trates the lowered vitality of the system, rather than the 

The same is true of all the other neurotic, rachitic and degen- 
erative conditions, hereditary or otherwise, that are met with, 
associate I with gingival inflammation. They all favor the 
occurrence of the disease by causing a weakened power of resist- 
ance predisposing to the attack of any irritation. The mouth, 
resistant as it ordinarily is, is at all times open to irritation. When 
resistance is impaired it gives way at its most vulnerable point,. 
and the gingival margin is one. Interstitial gingivitis is favored 
or hindered, like other disorders of its kind, by constitutional 
conditions which may or may not be inherited, and which bear 
toward it the relations only of predisposing and accessory 

1 Dental Cosmos, 1890, 



One of the most important factors of predisposition is that of 
degeneracy, either local or general. Three possibilities of life 
await, as has been elsewhere pointed out, 1 each living being : 
either it remains primitive and unchanged, or it progresses 
toward a higher type, or it backslides and retrogresses. The 
factors underlying the stable state force the animal to remain as 
it is ; these underlying the progressive tendency make it more 
elaborate, while the factors of degeneration tend to simplify its 
structure. Degeneracy is, therefore, a gradual change of 
structure by which the organism becomes adapted to less varied 
and less complex conditions of life. It is a reverse of develop- 
ment which proceeds from the indefinite and homogeneous to the 
definite and heterogeneous with a loss of explosive force due to 
the acquirement of inhibitions or checks. In proportion to the 
depth of degeneracy does it affect the earlier simpler, or later 
complicated, acquisitions. The opposite process of progression is 
a gradual change of structures by which the organism becomes 
adapted to more varied and more complex conditions of life. In 
progression there is a new expression of form corresponding to 
new perfection of work in the animal machine. In degeneracy 
there is suppression of form corresponding to the cessation of 
work. Elaboration of some one organ may be the necessary 
accompaniment of degeneracy in all the others. On the other 
hand, ' degeneracy in one organ may be the necessary accompani- 
ment to the elaboration in all the other organs. During the period 
of stress defects due to degeneracy are apt to appear and affect the 
line of least resistance, determined by the depth of degeneracy, 
as well as the variability of the structures concerned. As the 
teeth and jaws are among the most variable structures in the 
body, they are peculiarly apt to be affected by either general 
degeneracy, which affects the body as a whole, and has local 

1 Talbot : Degeneracy ; Its Causes, Signs, and Results. 


expressions or local degeneracy by which the body benefits. 
The factors producing degeneracy act by causing nervous exhaus- 
tion in the first generation. This implies a practical degenera- 
tion in function, since tone is lost. 

Every nerve cell has two functions; one connected with sensa- 
tion or motion, and the other with growth. If the cell lie tired 
by excessive work along the line of sensation or motion, the func- 
tion as regards growth later becomes impaired. The cell then 
not only ceases to continue in strength, hut becomes self- 
poisoned. Each of the organs (heart, liver, kidneys, etc.) has 
its own system of nerves (the sympathetic ganglia) which, while 
under control by the spinal cord and brain, act independently. 
If these nerve centers become tired, the organ fails to perform its 
functions, the general system becomes both poisoned and ill-fed, 
and nervous exhaustion results. In most cases, however, the 
brain and spinal cord are first exhausted. The nerves of the 
organs are thus allowed too free play, and exhaust themselves 
later. This systemic exhaustion has local expression in the 
testicle in the male, in the womb and ovaries in the female. 
Through this the body is imperfectly supplied with natural 
tonics (antitoxins) formed by these structures, and the general 
nervous exhaustion becomes still more complete. All the organs 
of the body are weakened in their function. Practically the 
neurasthenic in regard to his organs has taken on a degenerative 
function, albeit not degenerating in structure, since the rest- 
lessness of the organs is a return to the undue expenditure of 
force which occurs in the lower animals in proportion as it is 
unchecked by a central nervous system. Through the influence 
of various exhaustion agencies the spinal cord and the brain lose 
the gains of evolution and the neurasthenic is no longer adjusted 
to environment. Since the reproductive organs suffer partic- 
ularly, children, born after the acquirement of nervous exhaus- 
tion, are more or less checked in development as the influence of 
atavism is healthy or not — have degenerations in the structure 
of their organs which in the parent were represented by neuras- 
thenic disorder in function. As the ovaries of the neurasthenic 
woman generally exhibit prominently the effects of the nervous 
exhaustion, the offspring of these do not retain enough vigor to 
jiass through the normal process of development. 


The action of degeneracy, considered as a local factor of con- 
stitutional origin, may be exerted to preserve embryonic con- 
ditions in adult life. Such preservation may result in the 
breakdown of tissues which would otherwise withstand germs or 
other causes of disease external to the tissues. Given this con- 
dition of local degeneracy, a local predisposing factor is added 
to both the exciting causes and the constitutional predisposing 
factors. So long as the teeth and transitory structures remain in 
the comparatively stable condition of primitive races, this factor 
is to a great extent in abeyance. When, however, the jaw begins 
to evolve, the degenerate types find this factor adding dangers to 
their evolution. In the degenerate the struggle for existence 
between the organs is not properly balanced, whence the dangers 
from these local states of degeneracy that in the higher types 
are expressions of advance undergone without danger. This is 
excellently illustrated in the embryology of the mucous mem- 
brane. This in degenerate children often fails so to develop 
that the bactericidal function of mucus does not appear. This 
hereditary feebleness of the mucous membrane is peculiarly apt 
to occur in the nose, throat and gums, but other mucous mem- 
branes are not exempt. 



Miller, as elsewhere stated, found a little over thirty-three 
and one-third per cent on examination of twenty-six rachitic 
children under twelve years who manifested interstitial gingivitis. 
Considering that most of these manifested symptoms of inherited 
congenital or acquired constitutional defect, such a small propor- 
tion is rather remarkable. The fact suggests one of two explana- 
tions — either the children in the institute visited by Doctor 
Miller took better care of their teeth and gums than is usual 
with this class, or the cases in which pus existed only were 
classed as pyorrhoea. I have examined the mouths of deaf- 
mutes, blind, idiotic, feeble-minded and rachitic children in the 
institutions in America and Europe. Interstitial _ gingivitis was 
found in all its stages, from simple inflammation of the gums to 
loosening of the teeth, in from twenty-five to seventy-five per 
cent. In these cases not only are there constitutional factors, 
but also uncleanliness of the mouth and gum tissues. The 
degenerate children encountered in office practice usually have 
jaw deformities and teeth irregularities. Patterson has had 
under observation thirty-eight cases of well-marked pyorrhoea, 
thirty-three of which coexisted with nasal catarrh. These eases 
were, no doubt, those of degenerate patients. The nasal catarrh 
was a coincidence dependent on the general deficiency of the 
mucous membrane. 

Luxury and modern degeneracy are generally charged with 
the production of diseases later found to have attacked man 
in prehistoric periods. This has been the case with interstitial 

R. R. Andrews expresses the following opinion as to modes 
of life: "I have been led to believe from my own experience 
that this trouble exists largely in the mouths of people accus- 
tomed to luxury — good livers, people about middle age who. 
over-eat and under-work." 


No method of living can be regarded as a cause of this 
disease, except so far as it affects the general system, thus pro- 
ducing trophic changes. There is probably a slight difference 
in liability to interstitial gingivitis between people of sedentary 
habits and active outdoor workers, as well as between animals 
domesticated or in captivity and those which run at large. 

It is, however, obvious, from the data of the chapter upon 
tl History," that all races and stations, regardless of time, climate, 
or mode of life, have suffered with the disease. Examinations of 
animals in the American and European zoological gardens show 
that it is not confined to any class of animals. Dogs and cats, 
whether housed or running at large, suffer with it. 

The question how far this region is affected by toxic agents 
introduced into the system is an open one ; still it seems probable 
that they exert some influence. In chronic phosphorus poison- 
ing the jaw is particularly and seriously involved. This has 
been attributed chiefly to the entrance of phosphorus into the 
•deeper tissues through carious teeth or through solutions of con- 
tinuity of tissue due to tartar. In the case of other poisons this 
local factor is not so evident. Mercury has among its first 
effects a soreness of the teeth with loosening of them in their 
sockets. Here it appears that the alveolus was one of the first 
special points of attack independent of any traumatism or 
abrasion of the soft tissues. In a similar way the toxins of 
scurvy directly attack the alveolus. Its fleshy covering is later 
involved in the progress of the disease. This sometimes extends 
to complete loosening and falling out of the teeth. Here an 
irritation of a toxin from within the organism has a point of 
election, a structure that from its constitution or other reason is 
particularly vulnerable to attack. Another constitutional dis- 
order in which the alveolus is early affected is diabetes. The 
exact pathology of this is uncertain, but in many cases at least 
it is largely dependent on disordered action of the central nerve 
system. Renal disease is another common condition which tests 
the vulnerability of the alveoli. An ideally normal kidney is 
j^robably rare, but only when its abnormalities pass beyond a 
certain point can it be called diseased. In the less advanced 
conditions that have passed the line of morbidity, alveolar impli- 
cation is often very marked. This may be one cause of the 


unusual frequency in the insane, who are especially liable (as 
Bondurant ' and others have shown) to suffer from renal disease. 
They are very Liable likewise to auto-intoxications and trophic 
disorders as 2 well, since the balance of the nervous system has 
been disordered. Some (the paretic and organic dements) 
exhibit especial tendencies to trophoneurotic disturbances affect- 
ing the teeth. In states of depression and stupor, circulatory 
disturbances predispose to these. 

The constitutional results of acute and chronic infections are 
apt to produce auto-intoxicatioD in addition to the action of the 
toxins of their germs. The eruptive fevers, especially scarlatina 
or measles, have been long known to be followed by wasting or 
necrosis of the alveoli." Here the condition is notably symmet- 
rical and unaccompanied by exfoliation or necrosis of the osseous 
system elsewhere. Tuberculosis does not spare the alveolar pro- 
cess. The well-developed disorder known as Riggs's disease has 
been charged by Robin and Magitot to the direct influence of the 
arthritic (gouty and rheumatic) process, and declared a special 
form of arthritic manifestation. 

The alveolus is clearly vulnerable to the toxins of many 
infectious diseases. It is also quickly affected by some of the 
autotoxic influences of disordered metabolism. Its vital resist- 
ance to these agencies is less than that of other tissues. It is the 
earliest sacrifice when these toxins or all toxins disturb the har- 
mony of the organism. 

Another cause for implication of these parts than the action 
of toxins exists. Whenever tissue waste, whether local or gen- 
eral, exceeds repair there is trophic change. This latter depends 
directly upon disordered local or general nervous functions. 
Trophic alterations from the first cause appear in growth disorders 
of the nails and loss of hair (alopecia) after fevers — the most 
familial' obvious examples of this pathologic process. Of the 
other type are localized neurotic atrophies where the direct inter- 
vention of toxins can be excluded. The alveolus is liable to the 
first form of trophic deterioration. The influence of acute dis- 
eases upon the alveolus is probably thus exerted in many casts 

1 American Journal of Insanity, 1892. 
2 Kiernan, Journal of Nervous and Mental Diseases, 1878. 

J Salter : Transactions of Pathological Society, London, 1859-60, Vol. XI, page 309. 
Lucas, Lancet, 1887, page 692. 


rather than by direct infection. Where no cause has been ascer- 
tained, examination directed to this factor would probably reveal 
it. The general failure of the trophic centers after the prime of 
life (in senile states), which is attended with loss of teeth and 
wasting of the alveoli, is perhaps the most prominent instance of 
this type of trophic failure affecting the part. Even simple 
anaemia may thus rise to alveolar wasting. 

The second form of trophic failure in the alveolus is less 
prominent since it generally coexists with overshadowing disturb- 
ance elsewhere which masks it to a certain extent. C. Cruveilier 1 
noticed its occurrence associated with paraplegia and invokes a 
nervous influence in its causation. In facial hemiatrophy local 
wasting of the alveolus has appeared before the disorder had 
involved generally the jaws. This may sometimes be due to a 
local cause, but its occurrence and association with other neuro- 
trophic symptoms is suggestive. 

The causes which, acting locally, produce direct interstitial 
gingivitis, are the toxic effects of mercury, lead, brass, uric 
and other acids, potass, iodide, and other agencies acting in a 
similar manner, and scurvy. It is not the intention to enter into 
an elaborate discussion of the toxic action of these drugs, but in 
a general way to show the similarity in action and results upon 
the tissues. Scurvy, a disturbance of metabolism, produces the 
same train of symptoms as the metals. 

It is a widespread opinion among dentists that in toxic cases 
the gums are the first tissues involved. The fact is, however, 
that when the salts of mercury are taken into the system, as 
noted elsewhere, they act directly upon the central nervous 
system; later occur nausea and vomiting, tremor in the arms and 
hands. Besides local nerve inflammation (neurites), mercurial 
and brass poisoning produces paralysis agitans, and lead poison- 
ing, drop wrist, etc. 

Excessive secretions of the glands of the body, especially the 
salivary glands, later occur with rise in temperature, gingivitis 
with periosteal and j^eridental membrane swelling, thickening of 
the gums and loss of the teeth. The central nerve system dis- 
turbance affects all other structures. Inflammation of the 
mucous membrane of the mouth, as well as of the gums, and of 

1 Bak. Soe. de Chir. Paris, 1S70, pages 30 and 31. 


the alimentary canal, frequently occurs with sloughing of tissue. 
The kidneys become involved, and are unable to carry off the 
effete matter. 

The cachexia, which resembles that of scurvy, is characterized 
by great debility, anaemia, emaciation, alopecia, atrophy and 
coarseness of the nails, with pain in the muscles and joints. 

Mercury is eliminated by all excretory organs for which it 
has a great affinity. The soluble salts pass out by the bowels. 
So long as the excretory organs of the body eliminate mercury, 
the tissues are not effected. Small doses are eliminated, but con- 
tinuation of dosage soon involves the nervous system, and after- 
wards the tissues of the body, especially the jaw r s. The first 
effect of mercury upon dogs is to produce vivacity and animation. 
This lasts for two or three days, when the limbs begin to trem- 
ble. The kidneys and bowels act at first freely. At the end of 
seven or eight days paralysis agitans occurs. There is constant 
trembling, whether when awake or asleep; loss of appetite, with 
slight rise of temperature. At the end of two w r eeks, the gums 
become inflamed at the margins. If the drug be continued, 
death occurs in about three weeks. The loss of flesh is remark- 
able. Miners working in mercury mines, and looking-glass 
makers, are all affected to a greater or less extent. The nervous 
system is always involved. The kidneys become diseased. The 
hair drops out. The miners think it a happy issue from their 
trouble when they have lost all their teeth, or even the molars. 
They are henceforth exempt from suffering so far as the teeth 
are concerned. Many are toothless at thirty-five. 

Mercury taken by the mouth is found in the urine in two 
hours, and in the saliva in four hours. It appears in the urine 
fourteen hours after it has been applied to the skin. 1 Although 
it is believed to have passed entirely out of the system, it has 
been found in the brain, liver, kidneys and muscles. It is 
claimed that, like lead, it forms combinations with albuminoids 
in the tissues, for a time remaining inert, to be subsequently 
oxidized and returned to the circulation as an active poison. 
While a single dose of mercury may be rapidly eliminated from 
the system, repeated small doses distributed over a long period 
are not so eliminated on account of the thickness and occlusion 

Twentieth Century Practice of Medicine, Vol. Ill, page 935. 


of the walls of the capillaries, producing endarteritis obliterans, 
hence more or less of it is deposited in the tissue. 

Lead enters the system through the alimentary canal, skin 
and respiratory tract. A longer time is required to produce 
plumbism (lead poisoning) than mercurial poisoning. Lead is 
stored up in the system in minutest quantities for an indefinite 
length of time. Its effects are not manifest until the central and 
peripheral nervous systems have become involved, as evinced 
by the effect of plumbism upon the wrists. Occasionally, the 
chief seat of deposit is the liver or muscles. It is chiefly elim- 
inated through the kidneys, and very slightly through the liver 
and salivary glands. Not until a considerable length of time 
has elapsed is lead traceable upon the gums. This usually 
occurs about the lower incisors and cuspids. This deposit (lead 
sulphite) is always in the tissue outside of the blood vessels. 
Plumbism causes trembling, nausea and vomiting. The patient 
loses flesh, becomes anaemic, and has great resultant debility. 

The lead circulating in the capillaries accumulates, owing to 
impeded circulation resultant on a thickening of the coats of the 
vessel, producing occlusion. A bluish line upon the gums indi- 
cates that the system is completely saturated. Like mercury, 
lead collects in the mucous membrane upon the inside of the 
mouth, producing blue patches from a line to one-half an inch 
in length. Lead not only produces local irritation, but affects 
the peripheral nerves as well, producing trophic changes ; upon 
the capillaries a thickening of the inner coat results in endar- 
teritis obliterans. Brass produces, as Hogben 1 has shown, sim- 
ilar effects to mercury and lead ; the green gum is an early 

Potassium iodide exerts a like toxic influence to lead and 
mercury, as its pathology is similar thereto, but it is of infrequent 

Scurvy is due to poor food and hygiene. Insufficient alter- 
nation of food, impure air, want of bodily exercise, ennui and 
uncleanliness combine the causes of this disease. Previous to 
the introduction of canned goods, sailors on long voyages, 
prisoners and others under confinement were subject to scurvy. 
Lunatics, idiots or people who have had a long sickness, are now 

1 Birmingham Medical Review, 1887. 


most prone to it. Anaemic convalescents from protracted fevers 

suffer from it. 

In the British Arctic Expedition of 1875-76 over forty-eight 
per cent of the men suffered from scurvy. When the potato 
crop tailed in Ireland, in 1846, scurvy became prevalent. In the 
Crimean war 23,000 eases occurred among the French troops 
alone. Scurvy contributed over fifteen per cent to the death rate 
in the late civil war. It occurs among the Klondyke miners. 

In public institutions fur degenerate children it is very 
prevalent. I have observed it in both American and European 

Thomas Barlow 1 found scurvy associated with rachitis. Sun- 
derland" found that rachitic diathesis was a very strong factor. 
Jacobi reports forty cases of scurvy and rachitis. Babies in good 
families brought up solely on the proprietary infant foods are 
prone to scurvy. They lose their appetites, become pallid, per- 
spire freely, have diarrhoea, the mouth becomes sore with inflamed 
mucous membrane and gums. Purpura and haemorrhages of 
mucous membrane are common with pain and swelling of the 

In adults, excess of sodium chloride in the blood from con- 
sumption of salt meats and fish has been noted with scurvy. 
For this reason Rawls, of Cincinnati, Ohio, believed that an 
excess of salt in the system produced gingivitis. Languor, 
depression, amemia. with a rise of temperature, and enlarged 
joints with soreness are the first symptoms. 

The effects of this disease upon the system are almost identical 
with those of mercury and lead. Bruise-like (purpuric) erup- 
tions occur upon the skin and mucous membrane, on the serous 
membrane (notably the pleura, pericardium, meninges and 
synovial linings of the joints), mucous membrane of the mouth, 
stomach, intestines and bronchi. 

Owing to the anaemia, vascular weakness and altered compo- 
sition of the blood, oedema is common both in the lungs and in 
the submucous and subcutaneous tissue, especially the feet and 
legs. The gums begin to swell with redness and fibrous thicken- 
ing of the deeper layer, which cause protrusion, especially in 

'Medical Chir. Trans., London, Vol. CXVI, 1883. 
2 Practitioner, London, February, 1894. 


the cases of degenerates. The blood vessels, especially the capil- 
laries, become thickened, in some cases they are occluded, or ero- 
sion and ulceration occurs. The patient becomes decidedly pale 
and markedly debilitated. The skin is dry and blanched. Gen- 
eral emaciation is evident. 

The mucous membrane and gums become swollen and bleed, 
stomatitis ulcerans results in greater or lesser degree. The 
tongue is at first swollen, then it becomes dry and hard. The 
gums are at first reel and swollen. They bleed easily upon the 
slightest touch. Later they become pale and are irregularly 
larger, somewhat fungoid and friable, protruding between the 
teeth. They are quite tender to the touch. Ulcers appear on 
the buccal surfaces. The stomach becomes irritable, nausea and 
vomiting are common. Constipation occurs early and diarrhoea 
later appears. 

Factors acting through local trophic disturbances are not 
-only local disorders but also constitutional diseases, especially 
those which prevent elimination of effete matter (Bright's dis- 
ease, diabetes, etc.) skin eruptions, lung affections, auto-intoxica- 
tion (gout, etc.) and conditions like pregnancy, amenorrhcea, 
dysmenorrhea, etc. The physiologic processes of nutrition, 
growth and repair are regulated by local nerves which, as 
already pointed out, because of this function are called trophic. 
These are under control of both spinal and brain centers. Dis- 
orders of the local nerve or of the higher centers may produce 
trophic change. Such disorders affect more decidedly provi- 
sional structures, since the growth, nutrition and repair of these 
is normally unstable. The alveolar process is an outgrowth of a 
permanent portion of the skeletal structure, provoked and main- 
tained by the existence of what are really dermal appendages 
and not true bones. It is a provisional structure, almost unique 
of its kind in adult life, which has apparently little impendent 
vitality. This is in part due to mechanical causes, since its 
.slender structure unsupported by the teeth offers little resistance 
to impacts from without, to which its situation renders it espe- 
cially liable. There is more than this to be considered in reckon- 
ing the special vulnerability of the alveolus. It is protected by 
a thin layer of fleshy tissue only, which itself is peculiarly liable 
to injuries, thus exposing the bone to infection. There is, more- 


over, no cavity of the body that is more open to germs than the 
mouth, and some of these that arc considered ('specially viru- 
lent are its constant residents. Access of germs and accidental 
pathogenic factors to the alveolus is constantly afforded by cari- 
ous teeth, the irritation of tartar deposits, etc. Its liability to 
disease is thus indefinitely increased. As it is not very resistant 
to morbid influences, the infections have thus free play, hence 
suppurative disease is more readily induced. 

Great practical importance, as Hirt ' remarks, must be attrib- 
uted to the changes in the hair and teeth which are observed in 
tabetics (locomotor ataxia). The teeth become loosened without 
pain and fall out without appearance of inflammation ; the tooth 
being seemingly intact. This Hirt ascribes to disturbance in the 
nutrition of the jaw; an atrophic change connected with a lesion 
of the nucleus of the trigeminus. The fact that this condition is 
often connected with laryngeal crisis tends, in Hirt's opinion, to 
support the view of Buzzard 2 that the center for bone nutrition 
lies quite close to the vagus. Similar facts have been observed 
by C. L. Dana in America. 3 The conclusion is obvious that dis- 
turbance of the nerve centers governing nutrition, growth and 
repair exerts the same influence on the alveolus, jaws and teeth 
as similar disturbances do upon the skin, hair, mucous mem- 
branes and bones elsewhere. 

These structures, which have previously become affected by 
disease, although the patient has been restored to health, readily 
become the seat of interstitial gingivitis. This is illustrated in 
those persons who have been affected with scurvy, salivation, etc. 

1 Handbuch der Nervenkrankheiten, 1896. 
2 British Medical Journal, February 19, 1886. 
3 Diseases of the Nervous System. 



The technique of the examinations of interstitial gingivitis 
and pyorrhoea alveolaris in dogs was as follows : After fixing 
and hardening in two per cent formalin, alcohol, or Muller's 
fluid, the tissues were decalcified in a five per cent alcoholic solu- 
tion of nitric acid, imbedded in celluloidin and stained in various 
ways, the principal ones being hematoxylin and eosin. Ten or 
more slides would be obtained from each tooth. Out of these 
slides have been selected a series illustrating the progress of the 
disease from beginning to the loosening of the tooth. 

Fig. 31 is a longitudinal section of a cuspid tooth with the 
alveolar process in situ. A illustrates the enamel of the tooth, 
(E) the epithelium passes from the outer margin to the lower 
border, then folds upon itself and extends down the side of the 
crown of the tooth as far as the neck. Unfortunately, in this 
specimen, the structure connecting the epithelium and the fibrous 
tissue of the periosteum has been destroyed. The papillary layer 
of the sub-epithelial tissue is plainly shown at the outer border. 
Small round-cell inflammation may be seen extending along the 
border of this layer. It can also be observed extending down 
the capillary blood vessels into the submucous tissue (SI and G). 

Fig. 32 shows a similar section of another tooth. Here the 
epithelial structure (E) is pulled away slightly from the edge of 
enamel (A). In this section the infolding of the epithelium is 
shown at the neck of the tooth. This structure passes downward, 
folds outward and upon itself (AA) and returns two-thirds of 
the distance toward the gingival border, leaving a pocket (RR). 
The epithelium (E) is very dense and thick. The papillary 
layer of the submucous tissue (G) is very clearly defined. The 
capillaries (K) can be distinctly traced from the deeper fibrous 
tissue through the submucous layer into the papillary layer. The 
thick and heavy fibrous tissue of the periosteum (" Dental Liga- 
ment," Black) may be seen at H, inserted firmly into the 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 31. — Longitudinal Section of Tooth and Gum Tissue. Slight Gingivitis. Dog. 

A, Enamel. E, Epithelial Tissue. G, Submucous Membrane. M, Fibrous Tissue 
SI, Slight Inflammation. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced 

Fig. 32. — Longitudinal Section of Tooth and Gum Tissue. 
Gingivitis. Dog. 

Chronic Interstitial 

A, Enamel. E, Epithelial Tissue. G, Submucous Membrane. H, Periosteum. 
K, Capillaries. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peri- 
dental Membrane. RR, Space Pocket from want of Union of Epithelial Fold. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 33. — Longitudinal Section of Alveolar Process and Peridental Membrane. Slight 
Interstitial Gingivitis, Extending into Alveolar Process. Dog. 

J, Alveolar Process. 

Inflammation Extending through Enlarged Haversian Canals. 
I 1 , Inflamed Peridental Membrane. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 34. — Longitudinal Section of Alveolar Process and Peridental Membrane. Chronic 
Interstitial Gingivitis, Extending into Alveolar Process. Dog. 

H, Periosteum. J, Alveolar Process. V, Violent Inflammation. AA, Point of Union of 
Epithelial Tissue and Peridental Membrane. I 1 , Inflamed Peridental Membrane. L 1 , Inflam- 
mation Extending through Enlarged Haversian Canals. 


cementum and extending outward and downward. Just below 
( AA) may be seen the interlacing of the coarser fibers of the peri- 
osteum with the finer fibers of the submucous tissue. Chronic 
round-cell inflammation may be seen extending from the papil- 
lary layer through the capillaries into the interstitial tissue of 
the submucuous layer and the periosteum. Marked inflammation 
has occurred at Y. The openings in the folds of the epithelium 
are fruitful sources for the accumulation of food, epithelial scales 
and detritus, in which fermentation and decomposition from 
micro-organisms result, producing inflammation. 

Fig. 33 is a section through the peridental membrane (I) and 
alveolar process (J) at the lateral incisor. The inflammation has 
extended down from the papillary layer through the submucous 
tissue, the fibrous tissue of the periosteum into the peridental 
membrane and into the alveolar process. Round-cell inflamma- 
tion may be seen in the blood vessels extending through the 
Haversian canals (L 1 ). 

Fig. 34 is a similar section from another tooth showing chronic 
inflammation extending throughout the peridental membrane (I) 
and alveolar process (J). The Haversian canals (L) are well 
outlined by the inflammatory progress. Marked inflammation 
has resulted at V and also at the margin of the alveolar process. 

Fig. 35 is a section of the peridental membrane and alveolar 
process, illustrating the effect of interstitial inflammation upon 
the blood vessels and alveolar process. Chronic inflammation 
extends throughout the peridental membrane with very decided 
inflammatory change (V). The cut ends of the blood vessels 
which were originally situated in the Haversian canals are seen 
(BY). They have become involved with the result of a thicken- 
ing of the walls and endarteritis obliterans. The bone about 
these vessels has been entirely absorbed. The inflammation 
has extended beyond, into and through the Haversian canals, 
producing the type of absorption of the trabecular known as 
halisteresis ossium. Lacunar absorption has also occurred (O). 
Where decided inflammation (V) has taken place, abscesses are 
more liable to occur (as will be noticed later) from the large 
number of blood vessels at this locality. 

Fig. 36 is a section from another location of the alveolar 
process with a greater amplification, showing the inflammatory 


process extending through the alveolar process. Endarteritis- 
obliterans may be seen in different localities (EO). Three forms- 
of absorption are evident in this figure : Enlarged areas arising 
from absorption of the trabecular (halisteresis ossium) due to the 
inflammatory process. The vessels of Von Ebner precede perfo- 
rating canal absorption (BB), distributed over the entire field, also 
the result of the inflammatory process and lacunar absorption (O) 
which may result from inflammation. As long as the fibrous tissue 
remains in these large areas to retain the osteoblasts, new bone 
tissue may be produced under favorable conditions. On the 
other hand, when this tissue and the osteoblasts are destroyed, the 
alveolar process cannot be restored. 

Fig. 37 shows a section of the alveolar process from another 
dog. Here lacunar and other absorption (halisteresis ossium) are 
well shown. Thirty-seven osteoclasts (O) may be counted in the 
field while destruction of bone by halisteresis (Q) is rapidly 
going on. Remains of Haversian canals with the blood vessels 
may be seen (BY, L). In the discussion of the peridental mem- 
brane extending into the alveolar process (page 37), particular 
attention was called to the fact that large bundles of fibers 
extended into the process in such a manner as almost to isolate 
portions of bone. In the lower left-hand corner (X) may be 
seen two pieces of the alveolar process entirely separated from 
each other and the main body of the bone. In interstitial gingi- 
vitis, it is not uncommon to .find pieces of the alveolar process 
separated by halisteresis and lacunar absorption. When loose 
teeth are extracted as a result of this disease, pieces of the alveolar 
process come away with the peridental membrane attached to the 
tooth. Fig. 66 was obtained in this manner. In the upper left- 
hand corner may be seen eight or ten new osteoclasts (O) in an 
enlarged Haversian canal, at work isolating one piece of the 
alveolar process from the other. 

Fig. 38 shows a slide from still another dog. Halisteresis (Q) 
and perforating canal (P) absorption are here well shown. In 
the larger space at the lower left-hand corner may be seen two 
arteries (EO) which were originally the location of Haversian 
canals and which have thickened walls and a tendency to oblit- 
eration. The light color shows decalcification, the dark normal 
bone. At P may be seen perforating canal absorption. At FG 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 35. — Longitudinal Section of Tooth, Alveolar Process and Peridental Membrane. 
Violent Round-Cell Inflammation of Peridental Membrane, Extending through the 
Haversian Canals into the Alveolar Process. 

C, Cementum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. N, Large 
Spaces arising from Absorption of the Trabecule, starting in the Haversian Canals (Halistere- 
sis). 0, Lacunar Absorption. V, Violent Inflammation. BV, Blood Vessels, originally Haver- 
sian Canals. I 1 , Inflamed Peridental Membrane. L 1 , Inflammation Extending through 
Enlarged Haversian Canals. 

X 150. D. D. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 36. — Longitudinal Section of Alveolar Process. Chronic Inflammation Extending 
throughout, showing h alisteresis, perforating c.\nal and lacunar absorption. dog. 

J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecule, starting 
in the Haversian Canals (Halisteresis). 0, Lacunar Absorption. P, Perforating Canal 
Absorption. BB, Blood Vessels of V. Ebner preceding Perforating Canals. EO, Endarte- 
ritis Obliterans. 

X T.i. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
Fig. 37.— Longitudinal Section of Alveolar Process. Chronic Inflammation Extending 


J, Alveolar Process. L, Haversian Canals. N, Large Spaces arising from Absorption of 
the Trabecular, starting in the Haversian Canals. 0, Lacunar Absorption. Q, Halisteresis 
Ossium or Decalcified Bone. X, Remains of Calcified Bone. BV, Blood Vessels originally 
Haversian Canals. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 38. — Transverse Section, Alveolar Process. Chronic Inflammation Extending 
throughout. dog. 

J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecule, starting 
in the Haversian Canals. P, Perforating Canal Absorption. Q, Halisteresia Ossium or 
Decalcified Bone. X, Remains of Calcined Bones. EO, Endarteritis Obliterans. FG, Fat 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 39. — Cross Section of Tooth, A lveolar Process and Peridental Membrane. Chronic 
Inflammation of Peridental Membrane and Absorption of the Root of Tooth. Dog. 

B, Dentine. C, Cementuni. D, Pulp. I 1 , Inflamed Peridental Membrane 
S, Root-absorption. 

K, Capillaries. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 40. — Longitudinal Section of the End of the Root of a Tooth, Alveolar Process 
and Peridental Membrane, Showing Chronic Inflammation of the Peridental Mem- 
brane. Exostosis of the Root of the Tooth and Lacunar Absorption. Dog. 

C, Cementum. D, Pulp, with 3 Foramina. J, Alveolar Process. 0, Lacunar Absorption. 
P, Perforating Canal Absorption. CC, Cementosis. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 41.— Cross Sectio.v of Inflamed Peridental Membrane. Dog. 

II, Inflamed Peridental Membrane. \V, Epithelial Debris. 

X 15. 75M.M.ot>j. Spencer. Micro-photograph, reduced one-third. 

Fig. 42. — Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane, 
Showing Interstitial Gingivitis and Pyorrhcea Alveolaris, with Tooth About to be 
Exfoliated. Dog. 

C, Cementuni. E, Epithelial Tissue. H, Periosteum. I, Peridental Membrane. 
J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, Fibrous Tissue. R, Pus 
Pockets. U, Nerve Tissue. V, Violent Inflammation. AA, Point of Union of Epithelial 
Tissue and Peridental Membrane. CC, Cementosis. DD, Calcific Deposits Destroyed by Acids. 


X -10. 35M.M. obj. Zeiss. Micro-photograph, reduced one-third. 
Fig. 43.— Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane and 
Gum Tissue, Enlarged from Fig. 42, Showing Active Inflammation, with Pis Pocket. 

C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. I 1 , Inflamed Peridental 
Membrane. J, Alveolar Process. L 1 , Inflammation Extending through Enlarged Haversian 
Canals. MMnllamed Fibrous Tissue. R, Pus Pocket. V, Violent Inflammation. AA, Point 
of Vnion of Epithelial Tissue and Peridental Membrane. FF, Food Containing Micro- 

A. A. obj. Zeiss 

ro-phototrraph, reduced one-third. 

Fig. 44. — Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane and 
Gum Tissue, Enlarged from Fig. 42, Showing Active Inflammation with Pus Pocket. 

C, Cementum. E, Epithelial Tissue. J, Alveolar Process. M 1 , Inflamed Fibrous Tissue. 
R, Pus Pocket. V, Violent Inflammation. 


fat globules may be seen, while in the larger space at the upper 
right-hand corner is evident entire destruction of the fibrous 

Fig. 39 Illustrates a cross section of alveolar process and 
cuspid root, showing absorption of the, root. Inflammation 
extends throughout the peridental membrane (I). The capil- 
laries (K) are quite numerous. These are cut both crosswise and 
lengthwise. Absorption (S) of the root may be seen progressing 
at these localities. 

Fig. 40 shows a longitudinal section of the end of the root. 
Active destruction has been going on both in the pulp chamber 
(D) and at the external surface of the cementum (C). The irri- 
tation and inflammation has caused the odontoblasts to fill up the 
pulp chamber with secondary dentine, and obliteration of the 
chamber has taken place. Below the constricted pulp may be 
seen three divisions of the pulp (D) extending through three 
separate canals in the cementum (C). Cementosis ( CC ) may 
be seen at the end of the root. Lacunar absorption is going on 
(O ). Thus results a building up and tearing down of the same 
tissue from the same cause, interstitial gingivitis.. 

Fig. 41 shows inflammation of the peridental membrane (I 1 ) 
with epithelial debris (W) scattered throughout the field. 

Fig. 4_! is a section through the jaw and incisor tooth, showing 
the relation of the structures to each other in a severe case of 
interstitial gingivitis and pyorrhoea alveolaris. The tooth is 
attached at only a very small portion of the apical end of the 
root. The disease has been of long standing. Absorption of the 
alveolar process on one side has progressed on fully one-half of the 
root, while upon the other about one-third the distance. Inflam- 
mation commenced at the gingival border and extended through 
the periosteum (H), peridental membrane (I) and alveolar 
process (J). Marked inflammation (V) has occurred in the 
mucous membrane fold. An abscess has formed with a fistula 
extending to the gingival border. The thin border at the left of 
the fistulous tract is the epithelium layer next to the tooth. It is 
evident that the pus burrowed to the surface through the struc- 
ture instead of between the epithelium and the tooth. A similar 
abscess and fistulous tract are evident upon the gingival border 
on the opposite side of the tooth. The irritation produced by 


the movement of the tooth has caused the cementoblasts to 
deposit large quantities of material upon the sides and the end of 
the root. The main nerve trunks (U) may be seen at and below 
the end of the root. 

Fig. 43 illustrates the alveolar border on the right side of 
Fig. 40, greatly amplified. This shows the progress of intersti- 
tial gingivitis extending through the alveolar j)rocess producing 
absorption with intense inflammation of the peridental membrane 
and abscess with fistulous tract. 

Fig. 44 shows a similar process amplified from the left side of 
Fig. 42. It is interesting to note in this illustration that the 
fibers of the sub-epithelium pass down and become interwoven 
with the coarser fibers of the periosteum in just the opposite 
direction from those in the other side of the tooth, and in other 
illustrations. The fibers from the mucous membrane along the 
side of the tooth extend down and into the peridental membrane 
without a break in the structure. The arrangement of the fibers- 
of the submucous layer in producing the fold is well illustrated 
in the figure. This picture illustrates inflammation starting in 
the gingival border. 



To secure a chain of evidence that interstitial gingivitis (due 
to the metals, drugs, uric, lactic and other acids) commenced in 
the papillary layer of the sub-epithelial, mucous membrane, I 
instituted a series of experiments in mercurialization of dogs. 

Proj. ' 4 inch, ocular IS inch. Spencer. 

Fig. 45. — Longitudinal Section of Gingival Border, Showing Round-Cell 
Inflammation Due to Mercurial Poisoning. 

Dogs for the purpose were picked up in the streets. Some 
of these were operated upon by myself, but most of them were 
under treatment at the Post-Graduate Medical School. Care 
was taken to secure those in health and with healthy gums. 
Mercury was introduced by the mouth, skin and hypodermic 



injection. It was no easy matter to get them under influence 
of the drug, since the power of the glands to eliminate the poison 
was enormous. In no case was salivation produced. The first 
symptom noticed was exhilaration, which would last from three 
days to a week. Then paralysis agitans would continue until 
death. In about a week the appetite would commence to fail 
and it was difficult to get the dogs to take food of any kind. 
The kidneys and bowels eliminated the poison. There was a 


■)] ocular. No. 3. Leitz. 

Fig. 46.— Longitudinal Section ok Gingival Border. Higher Magnification, 
Showing Connective Tissue Infiltration with Plasma Cells and Polynu- 


rise in temperature. Some of the dogs died before gingivitis 
was observed. This demonstrated that not only does the nervous 
system become involved, but the organs of the body may be 
morbidly affected and death ensue before the gums show symp- 
toms of disease. Some dogs were killed after the gums became 
diseased. The time required to obtain results was from three to 
eight weeks. The age and physical condition of the dog caused 



this variation in time. After death the gum tissue was dissected 
from different parts of the jaws and placed in either fifty per 
cent alcohol, Miiller's fluid, or two per cent formalin. 

Sections of tissue from the gum margin and sides were made 
on a number of places. Some were imbedded in paraffin, others 
in celluloidin. The sections were stained according to various 
methods: Delafield's hematoxylin, eosin (Unna's), alkalin 
methylblue, carmin, Gramm's stain, etc. 

Fantachr. oil 1mm. ,'., inch ocular. No. 3. Leitz. 

Fig. 47. — Longitudinal Section of Gingival Border. Higher Magnification, 
Showing Round-Cell Inflammation Extending to the Inner Coat of the 
Blood Vessel and also Plasma-mast Ceils. 

Microscopic examination showed that the epithelial lining of 
the gums did not present pathologic changes, but appeared 
normal in every respect. Connective tissue below the gum 
epithelium (the tissue analogous to the papillary layer of the 
derma and the derma proper) presented unmistakable evidences 
of a mild inflammatory process. There occurred in this con- 
nective tissue round-cell infiltration, generally moderate hut in 


some places quite dense. This cellular infiltration extended 
from below (where it was densest) upward into the papillary 
layer (Figs. 45 and 46). The densest cellular infiltration 
usually occurred around the vessels (Fig. 46). 

Under high magnification, the cellular infiltration was found 
to consist of polymorphonuclear leucocytes, plasma cells and 

Projection U inch, ocular l'/ 2 inch. Spencer. 

Fig. 48. — Longitudinal Section of Gingival Border, Showing Round-Cell Infil- 
tration in the Connective Tissue and Extending into the Papill.e. Dog. 

plasma-mast cells, the latter with coarse basophilic granulations 
(Figs. 47 and 48). 

In some places were seen between the round cells, short, 
broad fusiform cells, the protoplasm of which took quite well 
basic methylblue. These cells resemble very much fibroblasts 
and appear to be derivations of the plasma cells (Fig. 49). No 
bacteria were found either in the areas of cellular infiltration 
(inflammatory areas) or elsewhere. In these cases it is obvious 
that there had occurred a mild inflammation of the gums (gingi- 



vitis). While this could not be seen with the naked eye, 
microscopic examination demonstrated histologic features of an 
inflammatory process. The absence of bacteria justified the 
belief that this inflammation was not of microbic origin, but due 
to mercury, which by its well-known chemotactic influence pro- 
duced the histologic changes of an inflammation. 

Pantachr. oil imm. ( ' a inch ocular. No. 3. Leitz. • 

Fig. .49. — Longitudinal Section of Gingival Border, Showing Round-Cell 
Inflammation Due to Mercurial Poisoning. Higher Magnification. 



The bacteric etiology of interstitial gingivitis has been inci- 
dentally discussed by many writers. 

Galippe 1 was probably among the first to make analytic 
experimentation in the bacteriology of this disease. He claims 
that there is found in the pus of pyorrhoea a parasite, resembling 
in shape the Greek letter N. Injecting this into the belly of a 
guinea pig, abscesses resulted, which had a special tendency to 
affect I tone tissue. Injections into the sjmce between the teeth 
and gums were negative in result. Galippe regards his experi- 
ments as suggestions for further research, but not demonstra- 
tive. Miller, 2 after explaining his own methods, made a series of 
culture experiments on agar-agar at blood temperature. Twelve 
cases of pyorrhoea in human beings, and six in dogs, were exam- 
ined. He isolated twenty different bacteria from human beings, 
and nine from dogs. Among the twenty kinds, staphylococcus 
pyogenes aureus was found twice. Staphylococcus pyogenes 
albus once, streptococcus pyogenes once. Of the other sixteen, 
nine subcutaneously injected produced no particular reaction, 
four a slight, three a severe suppuration in the subcutaneous con- 
nective tissue Among the nine species found in 

■dogs, staphylococcus pyogenes albus occurred once. Of the 
other eight, two subcutaneously injected caused no reaction, and 
five but slight. One caused very profuse suppuration, by which 
large portions of skin exfoliated Microscopic exami- 
nation of stained sections revealed masses of different bacteria, 
cocci and bacilli. Leptothrix occurred infrequently, and then 
■only on the surface of the cement, and where there were micro- 
scopical cavities in it Miller succeeded consequently 

in cultivating a large number of bacteria from pyorrhoea alveo- 
laris which possessed pyogenic properties, but was not able to 

Die InfectiiJse Arthro-Dentiiire Gingivitis, 1888. 
Micro-Organisms of the Human Mouth. 


determine the constant occurrence of any one which might be 
regarded as the specific micro-organism of pyorrhoea alveolaris. 
Miller remarks that it is not evident from Galippe's communica- 
tion whether he found the N or /S bacterium in all cases exam- 
ined, or hut once. 

Sudduth, after repeated examinations, arrived at the same 
conclusion as Miller. 

The results obtained in the Columbus Memorial Laboratory 
of Chicago, by W. A. Evans, were as follows: 

In order to determine whether a specific bacterium existed in 
the pyorrhoeic stage of interstitial gingivitis in man (necessary 
to constitute this stage a special disease), pus from more than fifty 
cases was examined. In all, the pus was obtained from the gums 
by a platinum needle under proper methods of sterilization. The 
pus from some cases was smeared on a slide. This was stained 
and such determination made as was possible with this proce- 
dure. With the pus from fifteen cases, agar was inoculated and 
placed in Petrie's dishes. The individual colonies were grown 
on gelatin, agar, bouillon, potato and blood serum. The results 
were as follows: In fifteen cases in which the organisms were 
plated out, fifty-five organisms were found. In two there was 
no growth. Two had but one species of germs, two had six, one 
had seven, and one had ten. The germs found are divisible into 
three classes: Those usually pathogenic to man, those excep- 
tionally pathogenic to man, and those never pathogenic to man. 
The first class was found thirty times, the second twelve, and the 
third thirteen. Class third is, no doubt, seemingly smaller than 
it should be, since many members of it probably do not grow on 
ordinary culture media. Of the germs most frequent ami 
important, staphylococcus pyogenes aureus occurred nine times, 
staphylococcus pyogenes albus six times, and staphylococcus 
pyogenes citreus once. A lanceolate diplococcus, growing like 
pneumonococcus, was found six times. Streptococcus pyogenes 
was found twice. Bacillus coli commune was found twice. A 
bacillus growing like the diphtheria bacillus occurred twice. 
This last bacillus had the appearance of the Kleb-LoefhVr bacil- 
lus. It lav on the slide like it and it stained irregularly. Of 
the less important organisms - , bacillus pyocyaneus was found three 
times, micrococcus tetragenus seven times, leptothrix seven times, 


bacillus mesentericus twice, bacillus subtilis three times. There 
was also present a peculiar large club-shaped fungus somewhat 
resembling the degenerative forms of actinomycosis. 

Did these examinations stand alone, definite conclusions could 
not be drawn from them. These, however, are admissible since 
all observations on this subject tend in the same direction. 
While, as already stated, Galippe believed that he had isolated 
two bacteria capable of causing pyorrhoea alveolaris, still he 
failed with both to produce the disease. This failure, according 
to the laws of Koch, is fatal to the position taken. 

M. Herzog, of the Chicago Polyclinic, on examination of 
cases of interstitial gingivitis, which had not reached the pyor- 
rhceic stage, had the following results : Pieces from the gum mar- 
gin which had been fixed and hardened in a formalin solution, 
were partly imbedded in celloidin, partly in paraffin. The sec- 
tions were stained according to various methods, including 
Gramm's, eosin (Unna's) and alkaline methylblue stain. The 
examination of the tissue shows an unchanged lining of stratified 
squamous epithelium, aud, in the connective tissue below the 
former, well-marked evidences of an inflammatory process. The 
round-cell infiltration is best marked in the deeper layers toward 
the periosteum, while the layers of connective tissue fibers nearer 
to the lining epithelium show less evidences of inflammation and 
are partly entirely free from any round-cell infiltration. The 
infiltrating round cells are of the type of lymphocytes, plasma 
cells and plasma mast cells. Very large and typical mast cells 
'are frequently found in the neighborhood of small vessels. 
Many of the vessels seen are quite tortuous, and the vascular sup- 
ply of the connective tissue appears to be considerably increased 
beyond the normal. Bacteria could not be demonstrated in the 
inflamed areas. 

M. Herzog's examination of the interstitial gingivitis, pro- 
duced by mercury in dogs, failed to reveal any bacteria. He was 
of opinion that the histologic changes of inflammatory type 
found, were due to the chemotactic influence of mercury and not 
to microbic action. 

In a paper 1 read before the Section on Stomatology of the 

'Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhoea 


American Medical Association, at Columbus, Ohio, George T. 
Carpenter mentioned some very interesting experiments in this 
connection. By infecting a fresh wound in the gums of rabbits 
with pyorrhoea and other pus he found the parts will remain 
infected only from two to five days. In other rabbits a rubber 
band was placed around teeth and pressed under the gums until 
inflammation resulted, when the parts were infected with pyor- 
rhoea and pus from a chronic ulcer; pus infection resulted. 

Like experiments were made in the human mouth on gums 
which had been neglected as well as on healthy gums, and with 
similar results. His experiments tend to show that, when animals 
and man are healthy, the tissues resist infection ; but when 
diseased, infection results. All yield to treatment. 

On examination of pus taken from pyorrhoea, pockets pro- 
ceeding from acute infection, two competent bacteriologists were 
unable to find a micro-organism not found in pus from other 
infected tissues. 

These results, in Carpenter's opinion, tend to show that a 
specific germ, to which pyorrhoea alveolaris is attributable, has 
not yet been found. 

The disease being so prevalent among dogs, it occurred to me 
that they would be of great value for experimental inoculation. 
The prevalence of the disease in dogs suggests that if it were a 
specific infection, these must be inoculable. Miller 1 had made a 
few inoculations of pus as well as of the deposits around the 
teeth. Slight inflammation, and, in one case, a little suppuration 
alone resulted. He afterward isolated twenty different bacteria" 
from the human mouth and nine from dogs. Some of the 
uncommon varieties were infective, but without marked results. 
Isolated varieties would probably not produce results that could 
be attained by inoculating animals with the fresh secretion (pus 
and other deposits) from dogs already affected with the disease. A 
dog was procured from the Veterinary Hospital whose gums and 
outer alveolar process w r ere almost entirely absorbed with pus 
exudate. Street dogs selected for inoculation were forty-six in 
number, ranging in age from one year to seven. They were of 
all breeds and conditions. Some were well fed, others very thin. 
Many had sound, healthy gums ; others had slight inflammation 

1 Miero-Organisms of the Human Mouth, page 329 


at different localities. No dog was used whose gums and alveolar 
process had become infected or whose tissues were absorbed. Two 
dogs were operated upon at a time. The gum was separated from 
the necks of the teeth down to the alveolar process and peridental 
membrane — one half at the canine, the other at the second 
pre-molar, since in a majority of cases the disease began at the 
canine tooth, probably on account of its prominence and the 
thinness of the alveolar process. The second pre-molar was 
selected because it is the least prominent. The secretions about 
the teeth and gums of the diseased dog were collected upon 
a platinum wire (previously sterilized) and conveyed to the 
injured parts. Thirty-nine healed in eight days. In these 
the gum tissues were healthy. The pus had no effect. The 
wounds healed as rapidly as any wounds possibly could. In 
seven the gums were inflamed and infection occurred. Suppura- 
tion was slight in four and considerable in three. The patho- 
logic findings in these cases were not unlike inflammation and 
infection in other tissues. Similar results would, no doubt, have 
taken place if inoculation had been performed with pus from an 
abscess. The last three dogs were allowed to depart at the end 
of four weeks with slight pus infection. 



While hundreds of slides could be adduced in support of this 
chain of evidence, sufficient have been given to permit of the 
introduction of evidence from other phases of the subject. 

The following- autopsy was made by L. Hektoen on an old 
man, in whose case the pathologic diagnosis was as follows : 
Senile marasmus (senile emphysema, senile sclerosis of the aorta, 
atrophy of the parenchymatous organs), scurvy (hemorrhagic 
gingivitis ) ; chronic aortic and mitral endocarditis ; fibrous 
myocarditis; chronic nephritis; caseo-calcareous areas in the 
right apex, spleen and left adrenal; double hydrothorax; bron- 
chitis ; fibroma of the stomach ; amputation of the left lower 
extremity at the lower third of the thigh. The findings unre- 
lated to the scope of the present investigation are omitted. The 
gums were found swollen, and here and there infiltrated with 
blood. There was purulent matter about the roots of the teeth, 
many of which were loosened and some of which could be 
removed with the fingers. The roots of the loosened teeth were 
covered with a granular grayish material. 

Bacteriologic examination of the root of the tooth gave the 
following results : Tube of bouillon from which agar plates 
were made, inoculated twenty-four hours before date, July 29, 
1898. There were two varieties of colonies: Both grayish white. 
One kind is round, pin-head size, slightly elevated, with thin, 
wavy, but sharply defined border. Finely granular. Media 
inoculated from one of these. Agar Slant: White, tallow- 
like growth along the track of the needle, with thin, more trans- 
lucent layer covering the rest of the surface. ( )nlv moderately 
elevated. Greenish tinge given to media. Potato: Elevated, 
"clumpy" growth, while on top, confined to needle track. 
Potato much darkened. Blood Serum: Gray, waxy growth, 
little elevated, sharply defined and thick border. Gelatin Slab: 
Saucer-shaped Liquefaction at upper part, more tubular in deeper 


portions. Flocculent masses throughout. Glucose Agar: Gas 
produced, white, thick growth on top. Milk: Alkaline, soft 
coagulation. Bouillon : Cloudy. Characteristics : Rapid growth, 
a sour, nauseating odor given off from all media, Morphology : 
Large coccus, single, in pairs and in groups. Stains easily by 
ordinary methods, also by Grams. The smaller colonies on agar 
plates (pin-point sized in center) with nearly transparent, illy 
defined peripheral zone. Border indistinct. Central portion in 
gray. Finely granular throughout. Agar Slant : Gray film 
over entire surface, somewhat thicker along the inoculation streak. 
At bottom there is a nearly white growth. Very light, greenish 
tinge to media. Blood Serum : Like on agar. Potato : Heavy 
dirty gray growth, wavy and sharply defined border. Looks like 
bunch of cauliflower. Gelatin Slab : Liquefied, saucer-shaped 
at top, tubular in deeper part. Growth mostly in upper stratum. 
Lit. Milk: Negative. Bouillon: Cloudy. Glucose Agar: 
Gas produced. Characteristics : Rapid growth, stinking odor 
from all media. Morphology : Small, slender bacilli ; actively 
mobile, spores. Takes ordinary stains readily and is not decol- 
orized by Gram's method. 

Only the lower frontal teeth and corresponding part of the 
jaw could be examined. The epithelial covering of the gums 
appeared to be quite intact. In some places it was a little thick- 
ened, and its lower layers infiltrated with new cells. The sub- 
epithelial tissue was much thickened, presenting the general 
structure of an inflammatory granulation tissue of some stand- 
ing. Areas occurred in which there were many new cells and but 
little stroma. In other foci the tissue was more fibrous, the new 
cells running in bands. Here and there occurred free and 
intracellular granular, yellow pigment, Typical hyaline bodies 
of various sizes, and staining a precise bluish violet with Gram's 
method, were found in rather small numbers. In some places 
small sub-epithelial abscesses were met with, which (in the instance 
of a district including a lower incisor) were really subperiosteal. 
The contents consisted of nuclear detritus and bacteria (mostly 
cocci) which have accumulated, especially upon and in the walls 
of the minute cavities extending from such an abscess. There 
seems to be a complete occlusion of the vessels (capillaries) with 
typical bacteria masses, staining a peculiar bluish violet color 

X 40. 35 M.M. Zeiss. Micro-photograph, reduced one-third 

Fig. 50. — Longitudinal Section of Tooth, Alveolar Process and Gingival Border, 
Showing Active Inflammation in Scurvy in Man. 

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. 

H, Periosteum. J, Alveolar Process. L, Haversian Canals. M, Fibrous Tissue. V, Violent 

Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Membrane. 
RR, Space Pocket from Want of Union of the Epithelial Fold. 

:::. MM. Zeiss. 

photograph, reduced one-third. 

Fig. 51. — Longitudinal Section of a Tooth, Alveolar Process and Gingival Border, 
Showing Active Inflammation in Scurvy in Man. 

B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. V, Violent 
Inflammation. Z, Sloughing of the Epithelial Tissue Due to Calcic Deposits. AA, Point of 
Union of Epithelial Tissue and Peridental Membrane. 

A. A. obj. Zeiss. 

iluri'il ont'-thivil. 

Fig. 52.— Longitudinal Section of Tooth, Alveolae Process and Peridental Membbane, 
Showing Blood Pigment in Blood Vessels of Peridental Membbane in Scurvy in Man. 

C, Cemenlum. J, Alveolar Process. K, Capillaries. I 1 , Inflamed Peridental Membrane. 
K 1 , Blood Pigment in Capillaries. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 53.— Longitudinal Section of Tooth and Gingival Boeder, Showing Active Inflam- 
mation Extending through the Mucous and Peridental Membranes. Scurvy in Man. 

B, Dentine. C, Cementum. E, Epithelial Tissue. V, Violent Inflammation. AA, Point 
of Union of Epithelial Tissue and Peridental Membrane. RR, Space Pocket from Want of 
Union of Epithelial Fold. M 1 , Inflamed Fibrous Tissue. 


with hematoxylin, and bine with Gram's method, so that the 
vessels presented the appearance of being very successfully filled 
by an infection mass : the small dilatations, the branches and the 
larger vessels (judging from structure these seemed to be veins) 
were sometimes brought out very nicely. The intravascular 
growth of bacteria extended into the bone below as well as, and 
more especially into, the peridental membrane. 1 These abscesses 
(suppurative periostitis) occur almost exclusively upon the inner 
surface of the alveolar process, being confined (as far as there 
was occasion to observe) to the external aspect of the process. 
There was always a thin, sound layer of bone separating the 
abscess from the peridental membrane. Very generally the 
spaces in the adjacent bone were filled with a cellular fibrous 
tissue in which occurred islands of osteoid tissue. The bone 
trabecule were generally covered by a thin layer of osteoid 
tissue, which (from the greater number of cells it contains, as 
compared with the other bones) must be newly formed. Rows of 
osteoblasts were found often upon the trabecule. Few How- 
ship's lacunae were found, and these were filled with small cells. 
There were no osteoclasts in the areas about the abscesses. The 
bone outside of the alveolar process is quite unchanged. 

The " bacterial thrombosis " not unusually extended into the 
peridental membrane, which then refused to stain as clearly as 
normal. The upper part of the peridental membrane was 
usually the seat of cell proliferation, and of the formation of 
fibrous tissue, due to the direct extension of the similar process 
in the sub-epithelial connective tissue of the gingivus. There 
were no indications that the process began below, at the apex of 
the tooth, for example, and extended upward. In the peridental 
membrane, and often connected with the cementum of every tooth 
examined, were very many so-called calcospherites ; calcified,, 
concentrically lamellated, round or oval bodies, not unlike the 
" corpora amylacea." In many instances, it seemed as if the 
body had formed in the cement or at its margin — the cement 
presenting here a nodular condition. 

Fig. 50 illustrates a section through the tissues of the jaw 

1 The abscesses have a definite outline or wall of ordinary cellular fibrous tissue 
displaying striking evidences of active inflammation. The tissue about the capilla- 
ries filled with bacteria refuse to stain clearly, but there are no signs of inflammation. 


and cuspid tooth. The epithelium is not so dense and thick as. 
in a similar section from the dog. Inflammation extends along 
the papillary layer of the submucous membrane (G) and involves 
the deeper structures. The mucous membrane layer has doubled 
upon itself, forming a pocket (R R). Violent inflammation is 
evident at A". This is of unusual interest, since it demonstrates 
that inflammatory products may be carried by the blood vessels 
anywhere throughout the alveolar process, and may result in 
abscesses. The inflammation extends throughout the periosteum 
(H), the fibers of which extend from the root of the tooth over 
the border of the alveolar process (J). There the coarse fibers 
of the periosteum contrast decidedly with the finer fibers of the 
sub-epithelium. Absorption and contraction of the alveolar pro- 
cess (fully one-half the length of the root of the tooth) has taken 
place, as well as lateral absorption. The inflammatory process 
extends through the Haversian canals (L). 

Fig. 51 is a section through the jaw at the lateral incisor. 
The epithelium (E) is seen upon the outer surface of the alveolar 
process as far as the root of the tooth. The inner fold next to 
the tooth has disappeared through encroachment of deposits 
which have been destroyed by nitric acid. Inflammation 
extends throughout the entire submucous membrane (G). The 
most marked inflammation in this case is entirely upon the 
outer border (V). 

Fig. .12 shows a section of the peridental membrane (I) 
and alveolar process (J). Capillaries (K) interlace through 
the field, the largest number being distributed along the 
alveolar wall. Blood pigment containing bacteria are notice- 
able (K'). 

Fig. 53 is an amplification of a section depicted in Fig. 50. 
This gives a clearer idea of the folding of the epithelium (E) 
and submucous membrane (G) layer upon itself, forming a pocket 
(RR), in which may be seen an accumulation of food and 
bacteria. It also shows extensive inflammation throughout the 
entiie field. Marked inflammation is evident at V. The point 
of union of the sub-epithelial layer and the periosteum is shown 

Fig. 54 illustrates inflammation of the peridental membrane 
with epithelial debris (W) scattered over the field, Endarteritis 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 54. — Cross Section Peridental Membrane, Showing Active Round-Cell Inflamma- 
tion. Scurvy in Man. 

C, Cementum. V, Violent Inflammation. \V, Epithelial Debris. EO, Endarteritis Obliterans. 

Fig. 55. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
-Cross Section of Inflamed Peridental Membrane. Scurvy in Man. 

I, Peridental Membrane. J, Alveolar Process. K, Capillaries. L, Haversian Canals. 
BB, Blood Vessels of Von Ebner Preceding Perforating Canals. EO, Endarteritis Obliterans. 
W, Epithelial Debris. 

x ;."i. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 56. — Cross Section of Tooth, Alveolae Process and Peridental Membrane, Showing 
Active Inflammation cnd Absorption of Bone. Scurvy i\ M w. 

C, Cementum. I, Peridental Membrane. J, Alveolar Process. P, Perforating Canal Absorp- 
tion. V, Violent Inflammation. 

X 40, 35 M.M. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 57.— Cross Section of Peridental Membrane and Alveolar Process, Showing Active 
Inflammation and Abscess. Scurvy in Man. 

Alveolar Process. T, Bacteria. Y, Abscess. I 1 , Inflamed Peridental Membrane. 
L, Inflammation Extending through Enlarged Haversian Canals. 

X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 

Fig. 58. — Cross Section of Peridental Membrane and Alveolar Process, Showing Active 
Inflammation and Another Larger Abscess. Scurvy in Man. 

J, Alveolar Process. P, Perforating Canal Absorption. V, Violent Inflammation. 
Y, Abscess. I 1 , Inflamed Peridental Membrane. L 1 , Inflammation Extending tbrougb Enlarged 
Haversian Canals. 

I Mil 



obliterans (EO) is also noticed at various positions. Marked 
inflammation may be seen at V. 

Fig. 55 illustrates a section of the peridental membrane (I) 
and alveolar process (J) with inflammation extending through- 
out. Capillaries (K) are also noticeable in large quantities, 
nearer the alveolar process than the root of the tooth. Epithe- 
lial debris are evident at W. Endarteritis obliterans (EO) may 

X 300. No. 2 projection ocular. D. D. obj. Zeiss. 

Fig. 59. — Cross Section of Tooth, Alveolae Process and Peridental Membrane, Showing 

Active Inflammation with Calcospherite in Membrane. Scurvy in Man. 

B, Dentine. C, Cernentum. I, Peridental Membrane. J, Alveolar Process. HH, Caleo- 
spherite. J', Inflamed Peridental Membrane. L 1 , Inflammation Extending through Enlarged 
Haversian Canals. 

be seen in different portions of the field. Inflammation has 
extended into the Haversian canals (L) but absorption has not 
occurred to any great extent. The blood vessels of Von Ebner 
(BB) are quite well shown. 

Fig. 56 is a section showing the cernentum (C), the peri- 
dental membrane (I) and the alveolar process (J). Marked 


inflammation extends through the peridental membrane, thence 
through the Haversian canals ( which are entirely obliterated ). 
Absorption of the trabecular (halisteresis) lias resulted to the 

extent that what remains of the alveolar process (J) are islands 
of bone held in place by the fibrous tissue. Blood vessels of 
Yon Ebner with perforating canals are seen at P. 

Fig-. 57 shows a section of the peridental membrane and 
alveolar process with a large abscess originally within the 
alveolar wall. Inflammation spreading through the peridental 
membrane has occurred at I', while the decalcified alveolar 
jjrocess is also shown (J). Violent inflammation has taken 
place within the alveolar wall, and an abscess ( Y) has formed. 
The wall of the ;d>sce<s is distinctly seen, with masses of bac- 
teria ( T ) clinging to the inner sides. The process of halisteresis 
(Q) (hone decalcification) is seen as a result of the violent 
inflammation. The entire wall next to the peridental membrane 
and about the abscess has been destroyed, and the different stages 
in the process by which this has been accomplished are beauti- 
fully shown. 

Fig. 58 illustrates a larger abscess (Y) from another loca- 
tion. This is also situated within the alveolar wall, showing 
that the inflammatory products extend through the blood ves- 
sels. Marked inflammation i> seen upon the side next to the 
peridental membrane (I'), while rapid absorption — halisteresis 
(Q) and perforating canal (P) — is proceeding at the borders 
of the abscess and nearest the alveolar process. 

Fig. 59 shows a section of a tooth (B and C), inflamed 
peridental membrane (I'), with absorption of the alveolar pro- 
cess {,]). In the inflamed peridental membrane may be seen 
a calcospherite. oblong in form. 



A forty-eight-year-old merchant was dyspeptic, debilitated 
and asthmatic, and for the treatment of these conditions he had 
been under calomel and tonics for a little less than two weeks. 
When he came under observation, the mucous membrane and gums 

were then much inflamed. There was marked sialorrhcea. The 
teeth were loose. The gums were swollen. Pus oozed from the 
gums. The breath had a decided metallic odor. At my sugges- 
tion, his medical attendant stopped the calomel. He was then 
ordered six pints of spring water daily. The gums were, on 
alternate days, saturated with iodin. In a few days the soreness 
and swelling were so reduced that the deposits could be removed. 
The patient was discharged cured in a short time other than as to 
the right inferior second molar, which was so loose as to require 
removal. This tooth was placed immediately in fifty per cent 
alcohol for twenty-four hours and then removed to absolute 



alcohol for twenty-four hours more. The membranes had 
receded about two-thirds the length of the root. Sections for 
microscopic purposes were made from the lower third of the root. 
Of these sections, Fig. 60 shows a small fragment of inflamed 
peridental membrane. Fig. 61 exhibits violent round-cell inflam- 
mation, degeneration and liquefaction of tissue. 

A thirty-five-year-old diabetic painter came under observation 
for plumbic poisoning. His gums were swollen. There was 
decided sialorrhoea. The teeth were loose. Pus flowed from the 

Fig. 61. 

gums. He was placed on ozonate spring water and the gums 
were saturated with iodin on alternate days. Three loose teeth 
were removed and placed in alcohol. Sections from the upper 
third of the left superior second bicuspid gave results on micro- 
scopic examination similar to those already described as occurring 
in mercurial poisoning. Fig. 62 sIioavs round cells of inflamma- 
tion. Fig. 63 illustrates very marked degeneration of the peri- 
dental membrane. In the lower right-hand corner are seen the 
root of the tooth, dentine and cementum. The whole surface of 



the peridental membrane is in an advanced phase of inflamma- 
tion. Just at the border of the root is evident an area of mem- 
brane softening. Just beyond, but joining, is noticeable breaking 
down of tissue. In the center are seen two areas of softened 
tissue more advanced in degeneration. 

One occupation disease which has been ignored in the etiology 
of interstitial gingivitis is "brass-workers' ague." In almost all 
brass-workers, a stain varying from a bright to a brownish green 
is detectable on the necks of the teeth between the crowns and 
the gum insertion. This is most obvious in the upper jaw. 
After a while, as E. Hooben 1 has shown, the teeth become 

loosened and fall out, Before these changes in the gum occur 
nervous symptoms have developed from the brass poisoning. 

Arsenic should be taken into account in the etiology of inter- 
stitial gingivitis. This drug has a very decided tendency in cer- 
tain subjects to cause, even in small doses, marked stomatitis and 
irritation of the mucous membranes throughout the body. 

Tartar emetic and the other preparations of antimony, produc- 
ing irritation of the mucous membranes of the mouth and else- 
where, may act as predisposing and exciting factors of interstitial 
gingivitis. 2 

1 Birmingham Medical Review, 1887. 

2 Lewin : Untoward Effects of Drugs. 



Among the drugs which should be taken into account in the 
etiology of interstitial gingivitis is potassium bromide. This 
produces in certain individuals, or when given to excess, marked 
increase of the saliva with irritation of the mucous membranes 
of the mouth, followed later by dryness of the mouth and shrink- 
ing of the gums. The bromides have, as II. C. B. Alexander 1 
has shown, a tendency to irritate all the mucous membranes of 
the body as well as the skin. Therefore, in dealing with cases 
of interstitial gingivitis in which the bromides are being taken, 
this factor should not be neglected. In these cases the symptoms 

Fig. 63. 

due to the bromides are apt to he charged to the nervous state for 
which the bromides have been given. The irritation of the 
mucous membrane by the bromides may occur quite early among 
the untoward effects produced by them. In all probability the 
bromine rather than the alkali is the source of these untoward 

What is true of the bromides is also true to an even greater 
degree, as has elsewhere been shown, of the iodides. 

1 Alienist and Neurologist, July, 1890. 



While, as already shown, the teeth originated in the epider- 
mis, still, even as early as the sharks, the teeth of the mouth 
departed from this primitive method of development, since they 
did not arise on the surface, but deep down, as Minot 1 has 
pointed out. As Hertwig has shown, this occurs because the 
dentiferous epithelium grows down into the dermis, forming an 
oblique shelf, which may be regarded as a special tooth-forming 
organ. On the under side of the shelf the teeth are developed 
in the same way as over the skin, although they are much larger. 
The teeth are, however, in various stages of development, and 
only one is fully exposed ; when, as happens in time, it is lost, 
the next tooth behind replaces it. Since the production of new 
tooth germs goes on in adult life, replacement of the tooth in the 
shark's jaw continues indefinitely; hence sharks are termed 
polyphyodont. Mammals, having two sets of teeth only, are 
called diphyodont. There is, therefore, even in mammals where 
the change is limited, a tendency to change. Since the human 
being and the higher mammals (noticeably the omnivora, like 
dogs, whose food is as varied as that of man) are born practically 
toothless, this struggle begins between the teeth at a later time 
than in the lower vertebrates. 

The teeth are temporary structures, intended to be shed at 
certain times ; the temporary set ere the onset of jmberty, the 
permanent with the onset of senile involution at the premonitory 
period of old age. This last period depends on the individual 
rather than the number of years lived. At the senile period, 
which may occur at any time after the eruption of the perma- 
nent set, osteomalacia (which is the normal absorption of the 
alveolar process) may take place. The period at which this 
commences depends upon the constitution of the patient, 
Through congenital defect or disease, senility may begin earlier 

1 Human Embryology. 


iii life. In certain types of degeneracy ( precocity, for example), 
senility with absorption of the alveolar process may begin even 
at twenty. Absorption of the alveolar process and loss of the 
permanent teeth, is, therefore, certain at a period dependent 
upon the constitution of the patient. Between these two periods, 
birth and senility, two sets of teeth have been furnished man. 
In the meantime, the alveolar process, the gums, periosteum, 
peridental membrane, blood vessels, nerves, have come and gone 
to suit the convenience of these two sets of teeth. Tissues Like 
these are called adventitious or transitory. Adventitious tissues 
are much more apt to be affected by disease than permanent in 
type and persistent in function. 

As transitory structures, destined to fulfill temporary pur- 
poses, the teeth of necessity tend to decrease in number with 
advance in development for the benefit of the organism as a 
whole, thereby preventing waste of nutriment on useless struc- 
tures. The shapes of teeth hence vary in order to adapt them- 
selves to the work and surroundings produced by evolution. 
The teeth and its setting being of different structures and com- 
position, each proceeds to destruction along lines imposed by the 
laws of its structure. The tooth is destroyed by decay, the 
alveolar process by inflammation. Decay of the tooth and inter- 
stitial gingivitis are expressions of that natural line of involution 
which is foreshadowed from the outset in both by laws of their 
development. The laws governing transitory structures natu- 
rally place these at the mercy of both under and over stimulation. 
From its position, location and functions the mouth is of neces- 
sity exposed to invasion of microbes. These tend directly and 
indirectly, from infection and through their toxins, to aggravate 
the effects of both under and over stimulation. Not only do the 
very structure and embryogeny of the teeth and alveolar process 
expose them to the too early onset of the processes of removal, 
initiated by under and over stimulation, but these last increase 
and are increased by the local results of constitutional defects, 
like idiocy, and diseases, like tabes dorsalis, paretic dementia, 
and allied disorders, as well as the results of injuries to the jaw. 

When more work is required of one tooth (as when the 
•dental arch is broken by the loss of one or more teeth, and the 
others have moved out of their normal position, or when a seam- 


stress bites her thread with one or more teeth, or when plates are 
attached or come in contact with natural teeth, or when a piece 
of bridgework is adjusted) and the roots of one or two teeth 
must support and do the work of a greater number, this charac- 
ter of adventitious structure predisposes to inflammation about 
the root or roots of the teeth. 

When due to irregularities of the teeth, or when antagonizing 
teeth have been extracted, or in the mouths of idiots, paretic 
dements, etc., who do not use their teeth, understimulation also 
predisposes to inflammation. 

The mass of evidence previously presented demonstrates that 
the causes of interstitial gingivitis are divisible into joredisposing 
causes (which may be subdivided into local predisposing and con- 
stitutional) and exciting causes. The exciting causes are either 
constitutional or local, but as a rule are local or have local action. 

The predisposing factors of this disease, as already men- 
tioned, are : conditions of jaw evolution, transitory nature of cer- 
tain structures, degeneracy and conditions of previous irritation 
and inflammation. 

Moreover, in accordance with a general law of pathology 
whereby tissues (for example the lungs in pneumonia once 
attacked by toxic agencies or even by the toxins of germs) 
acquire a local predisposition to future attacks of disease, the 
gums and alveolar process often become thus susceptible to con- 
stitutional and local influences. 

It is obvious from the data given in the chapter upon "His- 
tory " that interstitial gingivitis is as old as man and that it was 
observed and discussed by the earliest writers on medicine. 
While it is by no means improbable that constitutional factors 
assisted in its early progress in man, still the exciting cause of 
this disease was tartar. Many skulls from prehistoric periods 
exhibit gingivitis upon the teeth exposed to the influence of tar- 
tar. This gingivitis extends along the roots nearly or quite to 
the apices, resulting in absorption of the alveolar process. Upon 
the surface of the teeth where tartar is absent, interstitial gingi- 
vitis and absorption rarely occur. The same is true of the 
teeth of wild animals at large and confined in zoological gardens. 
In them gingivitis from local conditions, other than tartar, very 
seldom occurs. The jaws of the skulls of prehistoric periods are 


always broad, measuring '2:1') to 2.50 inches in diameter. Third 
molars are always present. The vaults are very low, the alveolar 
process short and thick, and the teeth short. As already shown 
in the chapter on the "Alveolar Process," the jaws have been 
growing smaller until they range in different races from 2.50 to 
1.75 inches in diameter. Mixed Celto-Teutonic J races, like the 
English-speaking peoples and the Scandinavian peoples, have the 
smallest jaws with the most marked deformities as a result. 
These changes in jaw forms occur, as has been elsewhere shown, 
in harmony- with the law of evolution of the race in face forms. 
With these changes in jaw diameter there also occurs an altera- 
tion in the antero-posterior diameter. A change in tooth forms 
also occurs. Small crowns and long roots replace large broad 
crowns and short roots. 

These changes necessarily alter the shape and form of the 
alveolar processes. Instead of being short and broad, they 
become long and thin. The septum between roots is not as wide, 
thick or heavy as formerly. The long, thin alveolar process is 
more subject to the influence of local irritation and trophic 
change than the short, thick one. A long, thin alveolar process 
will be more readily absorbed than a short, thick one. This is 
demonstrable where the roots of the teeth are situated near the 
outer border of the process. Disease of the peridental membrane 
and absorption of the 'outer plate extends along the roots, expos- 
ing them throughout their entire length. Similar conditions are 
noticeable along the palatine roots of the molar teeth in the 
upper jaw. 

From the length and thinness of the alveolar process result- 
ant on the evolution of the jaws, the periosteum on one side 
and the peridental membrane on the other hold the structures 
together and afford nourishment for the tooth and bone tissue-. 
The bloodvessels pass, as elsewhere shown, in a vast plexus from 
the periosteum to the peridental membrane through the process. 
This plexus deposits and removes calcium salts. Potent for good 
under normal conditions, it is equally potent for evil understates 
of irritation and disturbed nutrition. Local irritation is greatly 

1 Keane, Ethnology. 

2 Degeneracy : Its Causes, Signs and Results (Talbot). 

Osseous Deformities of the Head, Face, Jaws and Teeth (Talbot). 


assisted by a peculiar structural variation of the gum tissue (R 
R, see any figure); accumulation of debris and resultant chemi- 
cal decomposition producing inflammation. 

Tartar is an. active source of local irritation and inflammation 
of the gum margin. This in turn extends through the capilla- 
ries to the alveolar process. Calcic deposits are a result and not 
a cause. 

A predisposing cause for local inflammation is that of approx- 
imal tooth decay or cutting away the approximal surfaces for the 
purpose of filling this class of cavities. If the teeth be not so 
contoured (Bonwill) as to retain them in their proper positions, 
absorption of the alveolar process between the roots will take 
place, thus bringing the crowns in contact. The result of such 
absorption will restrict bone surface for the protection and nour- 
ishment of the gum tissue. Undernourished tissues are hence 
more liable to irritation and inflammation. 

When death of the pulp occurs, the teeth often become loose 
without inconvenience to the patient. This results from the for- 
mation of gases in the pulp chamber, which suffice to produce 
inflammation of the peridental membrane with or without pain. 
This occurs, since slight irritation only is needed to produce 
absorption of the alveolar process, at the apicial end of the root. 
Chronic inflammation of the peridental membrane and the 
fibrous tissue of the alveolar process occurs. The teeth finally 
become loose. Irritation from movements of the tooth increase 
the inflammation through the Haversian canals and further 
absorption takes place, until the tooth is exfoliated. 

This disease from the onset of gum inflammation may ftroceed 
for years without pain. Indeed, not until the formation of 
abscess, or until absorption has affected the nerve at the end of 
the root does pain occur. Slight soreness may be felt after the 
tooth begins to loosen. Absorption of the alveolar process and 
exfoliation of the tooth may occur without any pain whatever. 

In the chapter upon " Transitory Structures," it has been 
shown that the alveolar processes have their structures arranged 
to accommodate the teeth. When the teeth are extracted, the 
alveolar process becomes entirely absorbed. The periosteum, 
peridental membrane and fibrous tissues are entirely lost. The 
mucous membrane and gum tissue so contract that none of the 


original structure remains. Absorption of the alveolar process is 
very common in advanced age. Even when the teeth remain in 
the jaw in old age, whether of man or animal (this is especially 
noticeable in old dogs), absorption of the alveolar process con- 
tinues. This is due to the fact that the alveolar process, especially 
when long and thin, is composed of cancellated hone structure 
which is easily acted upon by its abundant blood and Lymph sup- 
ply. This produces absorption upon the slightest stimulation or 
irritation of nerve fibers. Even such slight factors as heat, brain 
overstrain, and want of proper articulation and occlusion and 
implantation of the teeth, suffices so to stimulate the nerve fibers 
as to produce absorption. There are four varieties of absorption : 
osteoclast or lacunar absorption, penetrating canal absorption, 
halisteresis, and osteomalaciary absorption. These have already 
been beautifully shown in the illustrations. It is. therefore, not 
astonishing that the slightest local irritation or tissue nutrition 
disturbance from constitutional causes suffices to produce local 
tissue change. This unstable condition of structures tends to 
prevent successful implantation of teeth. 

The question has arisen whether there exists a specific 
bacterium, which bears the same relation to the pyorrhoeic 
stage that the streptococcus does to streptococcus diphtheria. 
This question, raised by Galippe, must, in the Light of careful 
research, be regarded as settled in the negative. No special 
bacterium has been found which complies with the laws of Koch. 
Dogs are Liable to this disease. Galippe had but to infect their 
gums with his bacterium to demonstrate its specific pathogenic 
activity. Lie has not done this. As the researches (already 
cited ) also failed to find a bacterium which could comply with 
this test required by the laws of Koch, it must be admitted thai 
there is no bacteriologic evidence of a specific bacterium. 
Furthermore, the pathologic evidence demonstrates that bacteria 
play the very subordinate role in this disease that they do in 
ordinary wound infection. 


Inflammation of the gums and deeper structures chiefly 
results from mechanic and chemic (lactic and uric acid, potas- 
sium iodide, mercury, etc. ) causes, bacterial influence being an 


incidental complication. From their action, the blood stream is 
increased and dilatation of the capillaries is produced. The 
capillaries become crowded with blood corpuscles. These 
accumulate along the walls of the blood vessels, to which they 
apparently adhere. Accumulations of small, round cells occur 
in the submucous connective tissue, the spaces of which are 
filled with inflammatory exudate. The papillae become enlarged. 
The epithelial layer becomes hyperplastic. As a result, the gum 
tissues swell and become intensely crimson. They bleed upon 
the slightest touch. 

Inflammation may be confined to a single point upon the 
side of a tooth. This localization often results from predisposi- 
tion due to a local injury, originating in a cavity in the tooth 
with sharp, rough edges, from overlapping fillings or from too 
frequent and violent use of the toothpick at one point. As a 
result, granulation tissue forms, which (according to Sudduth) is 
often due to the irritation of lactic acid. 1 In the production of 
this, however, the influence of the lactogenic bacteria on particles 
of food cannot be excluded. 

The peculiar formation of the gum tissue on the inner border 
of the gingivus into a pocket or cul-de-sac (RR in Figures) here 
described for the first time, is a. fertile source of this irritation 
and consequent inflammation, from its collection of resultant 
decomposition of foods. This pocket varies, as has been shown, 
in size as well as locality. Sometimes it is very large and deep, 
or it may be almost, if not entirely, obliterated. Frequently it is 
situated near the gum margin, again near the union of the sub- 
mucous and peridental membranes. The degenerate epithelium 
cell structure (so-called glands of Serres) is also more liable 
and more easily irritated than the normal epithelium structure. 
As in the similar crypts of the penis, 2 the degeneration and 
death of the epithelial cells with which this cavity is lined 
produce by their accumulation a source of irritation as well 
as culture medium for pathogenic bacteria. Therefore, not 
only is the anatomical arrangement of the structures a fruit- 
ful source for the accumulation of irritative substances, but 

1 1 have made examinations of pockets about the necks of teeth and can cor- 
roborate this statement. 
2 Medicine, 1898. 


the structures themselves are also well adapted for inflamma- 
tory action. 

The gum tissue about one or more teeth may be injured by a 
badly fitted gold crown, with rough edges. The gold crown may 
he too tin- down on the i'oot. Injury may result from ligatures. 
rubber dam and hands left about the teeth after operations. 
Accumulations of tartar or any local irritation may lead to 
inflammation varying with the extent of the deposit. The extent 
of the inflammation will depend upon the nature and duration of 
the irritating influence. If it he local in action and temporary, 
slight gingivitis results. If it he permanent, gingivitis assumes 
a chronic type, extends into the fibrous tissue below and becomes 
interstitial in character. The extent of this interstitial inflam- 
mation depends upon the nature of the irritation. If the irrita- 
tion he located upon the side of one tooth, the inflammation will 
extend through the fibrous tissue in the direction of the course of 
the blood vessels. It may he in line with the peridental mem- 
brane. It may he in line with the periosteum, or it may he 
in direct line with the alveolar process. Interstitial inflammation 
( if one or more teeth be involved) extends not only through the 
peridental membrane, hut to the periosteum and alveolar process- 
as well, since the capillaries in surrounding structures are in- 
volved. The inflammation extends into the alveolar process 
through the Haversian canals and the blood vessels of You Ebner 
by way of the periosteum and peridental membrane. Irritation 
thereon resultant causes absorption of the alveolar process by ( a ) 
halisteresis, (h) Volkmann's perforating canals, ( <•) lacunar 
absorption (osteoclasts). The interstitial inflammation and the 
absorption of the alveolar process continues so long as the irrita- 
tion remains or until the tooth or teeth are exfoliated. Previous 
irritations often produce osteomalacia and trophic changes, and 
thus assist greatly the progress of the pathologic phenomena. 
Loosening of the tooth or teeth adds a very efficient irritation 
which increases the extent of and intensities the inflammation. 
Loosening of the teeth is their death knell, no matter what the 
original cause for the disease may have been. 

The following complications may occur: Endarteritis Oblit- 
erans, Absorption of the Alveolar Process, Pyorrhoea Alveolaris, 
and finally ( alcie I )eposits. 



Endarteritis is an inflammation of the internal coat of an 
artery or capillary, generally of chronic type. Its pathogeny is 
as follows : In direct contact with the blood streams is the 
endothelium (a layer of flattened cells); next is the tunica 
intima, composed of elastic fibers arranged longitudinally ; next 
comes the middle coat, composed of muscular fibers arranged 
transversely. The outer coat consists of longitudinal connective 
tissue, which contains the vasa vasorum. In the capillaries, the 
intima lies in immediate contact with the surrounding tissues, or 
accompanied by a rudimentary adventitia. tn other words, the 
walls of the capillaries consist of almost nothing but the intima. 
The capillaries have certain contractility; they contract or 
dilate without muscular fibers. The veins probably also have a 
certain amount of contraction and dilatation from irritability of 

Fig. 04. — Endarteritis Obliterans (Kauf.mann). 

A, Adventitia. E, Elastic Tissue between Middle Coat and Intima. M, Muscular. 
J, Thickened Intima, 

the intima. Each coat of the arteries takes on special type of 
inflammation. The causes of endarteritis are numerous. Inflam- 
mation of the intima of the blood vessels may be due to irritation 
from without or within. 

When it occurs from without, any local irritation will set up 
an inflammation which may extend to the outer coats of the cap- 
illaries. This produces a marked increase of blood. The vasa 
vasorum becomes swollen, the white blood corpuscles crowd into 
the terminal capillaries and migrate into the extra vascular 
space. Rapid proliferation of the round-cell elements takes 
place. The walls of the vessels become thickened. Owing to 
the projecting intervals of the intima, the caliber of the blood 
vessels diminishes (Fig. 04). 


Irritation occurring from within, results cither from trophic 
changes in the system from direct irritation from toxaemias, or 
from both interdependently. Under these circumstances a germ 
disease or other toxins may have an affinity for a certain organ, 
tissue or part, and produce irritation in the capillaries in a dis- 
tinct part of the body, or the capillaries through the entire body 
may become involved. Thus, in typhoid fever, the Peyer's 
gland in the intestine becomes involved; in scarlet fever, the 
skin or kidney ; in malaria, the liver and spleen ; in Bright's 
disease, the kidney ; while in mercurial and lead poisoning and 
scurvy, the mucous membrane, and especially the gums, become 
diseased. In many of these conditions, however, before the 
tissue already irritated becomes involved, the nervous system has 
become affected. The nervous system may already have become 
■affected from other causes. Thus, locomotor ataxia, traumatic 
injuries to the spine, paretic dementia, cerebral paralysis, neu- 
roticism and degeneracy, and last, hut not least, stomach neuras- 
thenia. The poison in the blood, together with the diseased 
peripheral nerves, produce irritation and inflammation of the 
inner coat of the capillaries. If this irritation does not disap- 
pear soon after its inception, the inflammation tends to affect the 
other coats of the blood vessels. ruder certain conditions, 
endarteritis may, however, never involve the other coats of the 
vessels. When irritation of the inner coat of the capillaries 
takes place, proliferation of the endothelium occurs. This 
inflammatory growth tends to obstruct the lumen of the vessel. 
The media may likewise become thickened by an increased con- 
nective tissue. The capillaries become obstructed, and finally 
obliterated. This finally impedes the circulation. Fig. 65 
shows such a condition in the scurvy case, elsewhere illustrated. 

Irritation may he of less intensity hut greater duration, as in 
case of syphilis, tuberculosis, scurvy, mercurialism, plumbism 
( lead poisoning), etc., and the results are then slowly effected. 
Proliferation of sub -endothelial connective tissue gradually 
increases until it reaches its limit (endarteritis obliterans). This 
influence of the proliferation is exerted in addition to that of the 
round-cell infiltration about the structure. 

The recent studies of Hektoen ' on meningeal tuberculosis 

1 American System of the Practice of Medicine, page 119. 



demonstrate that tubercle bacilli may penetrate the unbroken 
endothelial layers of the vessel and stimulate marked proliferation 
of the sub-endothelial connective tissue. An internal irritant, 
such as may be produced in the course of any infectious disease 
or from suboxidation, probably acts upon the endothelium of the 
walls of the smaller blood vessels in such a way as to permit the 
escape through the walls first of serum, then of leucocytes, the 

Fig. 6o.— Cr 
C, Cementum. D 

X ISO. D. D. obj. Zeiss. 
Section of Peridental Membrane, Showing Endarteritis 
Obliterans. Scurvy in Man. 

Dentine. I, Peridental Membrane. 
EO, Endarteritis Obliterans. 

IT, Nerve 

latter infecting and surrounding the vessels. The effect of the 
chronic endarteritis is to check the blood supply to the gum 
tissue. Mercury, lead and other poisons circulating through the 
blood are forced to remain, hence discoloration of tissue along the 
gum margin. Interstitial gingivitis, resulting in a slow disturb- 


ance of nutrition, produces overgrowth of connective tissue. In 
all cases of chronic interstitial gingivitis, as shown in the illus- 
tration, arc the blood vessels thus involved. 

Among the predisposing influences which cause this disease 
are syphilis, tuberculosis, mercurialism, plumbism, brass poison- 
ing, lithaemia, nephritis, gout, rheumatism, alcoholism, scurvy, 
nervous diseases, pregnancy and old age. Under certain con- 
ditions of the system any and all diseases which tend to lower the 
vitality, producing anaemia, will assist in producing this disease. 
The direct cause may be resultant overstrain of the blood vessels. 

Owing to obliteration of the arteriols in the alveolar process 
stasis of blood must follow. The detritus from the alveolar pro- 
cess, therefore, must remain in the tissue and collect upon the 
roots of the teeth. 


Absorption of the alveolar process is the result of irritation, 
resultant malnutrition, and subsequent inflammation. The osteo- 
blasts and osteoclasts are ever present to build up and tear down 
bone structure on the slightest provocation. Hypertrophy 
(building up of bone tissue) is the result of intermittent pressure, 
and atrophy, or absorption of bone, is due to constant irritation 
and pressure. As has been elsewhere shown, from its transitory 
nature the alveolar process is unusually susceptible to these influ- 
ences. The causes of absorption are loss of teeth by extraction, 
undue pressure upon one or more teeth from improper articulation 
(Bonwill), wedging and irregularity correction, heat under arti- 
ficial dentures, and interstitial gingivitis of local and constitutional 

According to Kaufmann, lacunar absorption is the most 
common type. This may be true in morbid anatomy of bone 
tissue generally, but it is not true of absorption of the alveolar 
process. On an examination of hundreds of slides prepared 
from canine and human jaws (of which characteristic types arc 
illustrated), by far the most common form of absorption was 
found to be halisteresis. Perforating canal absorption, which 
Kaufmann has "occasionally met with," is certainly very com- 
mon, while lacunar absorption holds third position. This order 
of absorption is accounted for by the fact that where structures 


are transitory, halisteresis, as quickest method, follows by the law 
of the survival of the fittest. For the same reason perforating 
canal absorption should stand second. • The blood vessels of Von 
Ebner being most numerous, although considered smaller, they 
would naturally be the second tissue involved. As in interstitial 
gingivitis, absorption of the alveolar process is invariably due to 
inflammation, halisteresis apparently starts at the larger Haver- 
sian canals from which this form of absorption invariably 

Interstitial gingivitis extends to the alveolar process through 
the periosteum as well as the peridental membrane (not, as den- 
tists usually believe, by way of the peridental membrane alone). 
This is demonstrated by the illustrations. The entire alveolar 
process thus becomes involved. The products of inflammation 
extend through the Haversian canals (a path obviously evident 
in pathologic illustrations), setting in action the three forms of 
absorption as elsewhere illustrated. 

Halisteresis Ossium ( doXo? of salt, ere/tims deprivation ) or 
decalcification, is that process of absorption wherein solution of 
the lime salts first takes place, while the cartilage or matrix 
remains for the time undisturbed. 

Solution of the lime salts begins at the periphery of the 
Haversian canal and advances toward the center of the tra- 
becule. This absorption follows, as a rule, the bone layers. Bone 
centers are, therefore, usually the last to be absorbed. Fre- 
quently decalcification becomes complete; nothing remaining but 
the organic matrix or cartilage. Finally, this is also entirely 
destroyed. As the osteoblasts occur in the matrix or cartilage, 
it is not difficult to understand that absorption may extend far, 
yet restoration of the alveolar process may occur. After destruc- 
tion of the matrix such a restoration is impossible. New fibrous 
tissue may be partly restored, but it is doubtful if the alveolar 
process can be. 

Both Ziegler 1 and Kaufmann 2 divide osteomalacia into senile 
and juvenile. The latter occurs most frequently during jjreg- 
nancy. In senile absorption, after a certain period, the entire 
skeleton is affected. The condition begins most frequently in 

1 Special Pathological Anatomy, page 151. 
2 Pathologische Anatomie. 


the "vertebrae and thorax; Inter extending to the extremities." 
In pregnancy "the pelvic bones are first involved, the process 
then extends to the other bones." It is singular that the alveolar 
process should have been so much neglected by pathologists, 
since, in both states, the alveolar process becomes involved long 
before the bones of the body. 

This is due to three reasons: first, to trophic changes; sec- 
ond, to the alveolar process being a transitory structure; and 
third, to improper care of the gums at these periods. 

Osteomalacia occurs in the alveolar process much earlier than 
at the so-called "senile" period. It is found at twenty, or even 
earlier. At any period beyond that year, it occurs probably from 
the prematurely senile states of which precocity is a type. The 
lost tissue is regained often after confinement in the " preg- 
nancy" type, but is never regained in the senile. 

The causes which produce morbid decalcification are not thor- 
oughly determined. Some believe it to be due to lactic acid in 
the system, others attribute it to an increased amount of carbonic 
acid in the blood. Eisenhart believes it to he due to a want of 
alkalinity of the blood, while Von Reehlinghausen charges it 
to a local irritation of the vascular mechanism of the bones. It 
would seem, from examinations already cited, that, so far as the 
alveolar process is concerned, local irritation from biochemic 
changes in the blood, as suggested by Von Rechlinghausen, i> 
the chief cause. Premature absorption of the alveolar process 
accompanies the movement of the teeth in their correction or in 
rapid wedging. Frequently the alveolar process is never fully 
restored, thus producing a predisposing factor for future disease. 

Premature absorption, or osteomalacia of the alveolar process, 
is easily recognized. A shrinking of the gums and alveolar 
process exposing the necks of the teeth is very conspicuous. 
Frequently the gums and mucous membrane covering the alveo- 
lar process is quite red (this is very noticeable in dogs), and a 
thinning of the alveolar process over and between the roots of 
the teeth. The process of one tooth only may become involved : 
again the process over two. or the whole jaw. and again both jaws 
become affected. 

When osteomalacia occurs, either of pregnancy or senile 
type, although the tissues he seemingly restored to health, struc- 



tural change has taken place to such an extent that it ever 
remains a predisposing factor to interstitial gingivitis. 

In Fig. 36 may be seen the blood vessels of Von Ebner. 
These blood vessels are also to be observed in Fig. 55. They 
are very common in the alveolar process and, according to Volk- 
mann, are the source of the perforating canals which bear his 

X ?>o. !i-ineli obj. No. Oe. 

Cross Section or Tooth, Alveolar Process and Peridental Memrrane, 
Showing Lacunar Absorption. Man. 

Fig. 66, 

C, Oenientuin. D, Dentine 

I, Peridental Membrane. 
0, Lacunar Absorption. 

J, Alveolar Process. 

These canals run in all directions. After absorption has gone 
on to form medullary spaces, these canals penetrate through the 
trabecule from one space to the other (Fig. 38). The position of 
this type of absorption in the order of frequency conies from the 
fact that, in this disease, absorption is almost entirely due to 



inflammation ; hence the blood vessels are the first to become 
involved. Those entering the Haversian canals, being the larger, 
are first affected, and hence halisteresis naturally precedes. 

When irritation takes place in a nerve or part of hone which 
is about to he absorbed, multinuclear cells arise at the border in 
the periosteum and peridental membrane. They attach them- 
selves to the surface of the bony trabecular. According to Sud- 
duth, "the absorber and the absorbed must be in touch with each 








x 300. No. 2, projection ocular. D. D. obj. Zeiss. 
Fig. »>7. — Section of Peridental Membrane, Showing Lacunar Absorption in Dog. 
.1, Alveolar Process. O, Lacunar Absorption. I 1 , Inflamed Peridental Membrane. 

other." Kolliker has named these cells "Osteoclasts," which 
term has come into general use. Very soon after these cells 
make their appearance, cavities are seen in the hone tissue. 
These cavities are called Howship's lacuna?. Lacunar absorp- 
tion, as elsewhere shown, takes place as a result of irritation and 
overstimulation. Fii>\ 66 shows a cross section of the end of one 


of the buccal roots of Fig. 68. As will be observed, this tootli 
was held in place by two buccal roots. As much resistance was 
required of these two roots as was formerly required of three. 
Irritation due to excessive force in mastication was causing 
absorption. Round-cell inflammation is not present in the peri- 
dental membrane. The irritation may be continued until inflam- 
mation sets in and until the bone is entirely absorbed, as noticed 
in Fig. 67. Small round-cell inflammation is quite noticeable in 
the surrounding tissue. 

Sometimes these lacuna? may be -seen extending along the 
entire length of bone. As many as thirty-seven may be counted 
in some fields (Fig. 37). Lacunar absorption frequently so 
extends through the Haversian canals as to cut off pieces of the 
alveolar process. A casual glance at Fig. 66 demonstrates this. 
This figure could be multiplied many times from other slides. 
These frequently come away with the peridental membrane when 
the tooth is extracted. This is often noticed in removing loose 
teeth due to interstitial gingivitis. By passing the finger over 
the surface of the root, the rough pieces of bone may be easily 

Aside from the forms of absorption already noted, absorption 
of the alveolar process is often seen, the result of neuropathic 
lesions. Paretic dementia, diseases of the spinal cord, low forms of 
inflammation, general debility and traumatism, together with 
unhygienic conditions of the mouth, are fruitful sources of inter- 
stitial gingivitis and absorption of the alveolar process. Absorp- 
tion of the alveolar process takes place also in diathetic diseases 
in which the nervous system has been involved (syphilis, scurvy, 
lithsemia, etc. ). 


Recovery from interstitial gingivitis and return to normal 
conditions without change in structure is called restoration. 
Should the damage be extensive, and accumulations of cell and 
liquid exudate so press upon the tissues as to extinguish their 
vitality, ordinary restoration is impossible. This is also true 
when the inflammation is more decided and persistent. This 
inflammation may extend throughout the tissue. Absorption of 
the alveolar process may take place, and exfoliation of the teeth 


result without pus infection. The tissues may be in a favorable 
condition for infection, yet the mouth and blood vessels be free 
from pus germs. This is not uncommon. The tissues are often 
invaded, however, by micro-organisms, resulting in suppuration. 
Interstitial gingivitis, with pus infection in and about the alveolar 
process, resembles suppuration elsewhere in the body. It results 
either in an abscess or ulceration. An abscess is a collection of 
pus within the tissues. Ulceration is a collection of jms upon 
the surface of the tissues. Both of these marked conditions. 
being dependent upon inflammation, are associated with intersti- 
tial gingivitis. 

Suppuration (due to pyogenic cocci) is the usual termination 
of infective inflammation. Healthy gum tissue is intolerant of 
bacteria, and will resist the invasion of micro-organism. When 
inflammation takes place, the diseased part is unable to resist 
them. Lowered vitality of tissue is a fruitful source of infection 
and suppuration. Since, as Miller 1 has shown, pus germs are 
found in almost every mouth, infection is a very probable outcome 
of gingivitis. 

The organism most frequently producing pus are the staphy- 
lococcus pyogenes aureus, and albus. These have a tendency to 
accumulate in groups. When they collect at a given point in the 
tissue, suppuration results. The streptococci ( occasionally pres- 
ent in the mouth) do not as a rule produce local suppuration, but 
spread through the tissue by way of the Lymphatics and blood 
vessels, and eventually give rise to abscess. The delicate reticu- 
lum of the blood vessels found in the Haversian canals is a 
convenient lodging place for swarms of bacteria, owing to the 
slowness of the blood current and the tortuous course of the 
blood channels. When 2 the circulation has been impeded or 
arrested by an extravasation of blood or congestion of a part, the 
conditions are favorable for intravascular infection if organism 
happen to be circulating in the blood at the time. As we have 
-ecu, micro-organisms may from time to time be found in the cir- 
culation, particularly in individuals of feeble constitution. The 
anatomic nature of the part will therefore determine suppuration 
in certain localities. 

Micro-Organisms of the Human Mouth 
American Text-Book of Surgery. 


In whatever part or tissue the change may occur, the process 
is the same. The original structures disintegrate. Their place 
is taken by a closely packed crowd of migrated leucocytes. 
Should the cause continue to act, the process culminates in the 
formation of pus. The migrated cells cut off from proper 
nutrition by pressure are exposed to the injurious action of 
micro-organism. The central cells of the group degenerate from 
want of nutrition or die from direct action of the irritation. The 
intercellular substance softens, and the liquid exudate from the 
surrounding parts mingles with the broken-down tissue to form 
an abscess. 

As I have shown, foci of infection and intense inflammation, 
to the point of degeneration and liquefaction, occur in most 
every locality within the peridental membrane, periosteum and 
alveolar process. These abscesses are just as likely to point 
upon the surface of the gum as on the inner surface next to the 
root of the tooth. When abscesses form in and about the 
alveolar process, with fistulas opening outside of the inner 
alveolar wall, the disease cannot be entitled pyorrhoea alveolaris, 
since, as elsewhere shown, strict definition of this title implies 
pus flowing from the alveolus. 

Abscesses which discharge their contents into the space 
between the alveolar wall and the root of the tooth, and ulcer- 
ation of the peridental membrane only, could literally be con- 
sidered under the head of pyorrhoea alveolaris. 

Abscesses in and about the alveolar process (other than those 
due to dead pulps) are very common. This is due first to the 
unstable condition of the structures, and second to the ready 
access of pus germs through the inflamed gums and peridental 
membrane. Those most susceptible to infection are patients who 
are anaemic and below par in vitality, and whose gums have 
become inflamed either from local or constitutional causes. 
Especially is this the case in those who have osteomalacia 
where the gums have receded quite a distance from the necks 
of the teeth. Pus germs collect at the necks of the teeth, infect 
the raw inflamed surfaces of the epithelial layer, and entering 
the circulation are carried into the deeper structures. Intense 
inflammation results. Abscesses form, discharging their con- 
tents upon the surface. Pus germs also enter the deeper struc- 
tures through exposed pulps. 


Two cases of interest in this connection occurred recently in 
practice. An active business man, fifty-five years of age, pre- 
sented himself with an abscess over the buccal roots of the left 
superior second molar. There were no dead pulps in any of the 
teeth upon that side of the jaw. Absorption <>t' the alveolar 
process and contraction of the gums had occurred around all the 
teeth. He had been overworked and was nervously exhausted. 
Five years ago cataracts were removed from both eyes. He is 
exceedingly sensitive to pain. Examination of blood revealed 
slight anaemia. On examination of urine, other than a specific 
gravity of 1028, it was found normal. The abscess was lanced 
and cavity cleansed. It healed within a week. Subsequently 
he returned with another abscess over the root of the right 
superior central incisor. Live pulps were in all the teeth upon 
this side as far as the second molar. Infection, therefore, must 
have occurred through the gum and peridental membrane. 

The teeth of a lady forty-six years of age were being put in 
order; after filling a cavity, May 14, 1899, she called attention 
to a space between the second and third superior right molars, 
and stated food lodged at that point, causing pain and bleeding. 
The space was cleansed with an excavator and the cavity 
syringed with warm water and then explored. Absorption of 
the gums and alveolar process had extended one-half the length 
of the buccal root. Applications of iodin were made to reduce 
the inflammation. The patient was dismissed with an appoint- 
ment for May 17. She returned at the appointed time with an 
abscess over the palatine root as large as the thumb. The lady 
had had acute pain from the time she left the office until her 
return. The parts had been infected with pus germs through 
the peridental membrane. The pus was collected in a tin tea 
spoon, from which cultures were obtained and glass slabs 
smeared for microscopic examination. The pus was examined 
by George T. Carpenter for calcic deposits ; the usual aseptic 
precautions having been taken. 

Microscopic examination revealed the usual pus germs. 
Chemical analysis for calcic deposits in the pus was made as 
follows: The pus was placed in a test tube with hydrochloric 
acid (diluted with four times its bulk in water). The phosphate 
is dissolved. It is then diluted with water, boiled, and when 


cold excess of solution of ammonia added. The lime salts are 
then re-precipitated as an amorphous powder. 

Many dentists, ignoring the laws of pathology, insist that 
intense inflammation in remote parts of the alveolar process is 
not due to invasion by micro-organisms of an inflamed tissue, 
but is the result of gouty deposits. The utter lack of foun- 
dation for this theory must be apparent on the slightest study 
of pathology. 

Ulceration is always located upon the surface of a tissue. 
When ulceration occurs from contact irritation of the gum margin 
or by mechanical or chemical means, congestion and oedema 
result, thickening of the epithelial layer and increased growth of 
cells. The sub-epithelial tissue becomes inflamed. The process 
is not unlike that of the formation of an abscess, since the 
infected tissue resembles part of an abscess wall. In slowness of 
progress only does ulceration differ from acute inflammation. 

Such is the condition of the peridental membrane. When 
simple gingivitis becomes chronic, the inflammation extends to 
the surface of the peridental membrane. This is situated at the 
Lower extremity of a cul-de-sac, formed by the gum on the one 
hand and the tooth on the other. This cavity is filled with 
foreign material in which decomposition continually occurs. 
The tissues are thereby constantly irritated. Necrosis occurs at 
the surface. In the deeper tissues that' have become inflamed 
pus cells also are found. These not only arise from the normal 
blood vessels in the vicinity, hut also from the granulation tissue. 
The causes of peridental membrane ulceration are disturbances of 
nutrition, endarteritis obliterans (a disease of the blood vessels 
due to constitutional diseases, such as syphilis, scurvy, tubercu- 
losis, uric acid and other blood poisons) and starvation of tissue, 
feeble circulation (as in anaemia) and inflammation. If the 
ulcerated surface be examined under the microscope, a general 
thickening of the tissues will be seen. In the papillary layer 
deposits of blood pigment (Fig. 52)' occur. The surface is 
covered with granulation tissue. The tissue may, in part, 
resemble the type of healthy granulation. It is composed of 
round cells closely packed together and supplied with rich capil- 
lary network. Coagulation necrosis from breaking down of 
granulation tissue may be present. 



The influence of the stage of interstitial gingivitis known as 
pyorrhoea alveolaris on the system has been discussed by John 
Fitzgerald. 1 He points out that pyorrhoea alveolaris may act in 
three different ways in the causation of systemic disease. The 
pus, with its multitude of putrefactive organisms and decayed 
food remnants from the pus pockets, may be swallowed and either 
act locally upon the stomach wall or set up fermentation of the 
stomach contents. The toxins generated in the month may be 
absorbed by the mucous membrane of the mouth or stomach and 
thus pass into the general circulation. The local conditions of 
the mouth may favor the growth of pathogenic organisms, and 
thus render the patient more liable to certain infectious disorders, 
noticeably influenza. The power of pyorrhoea alveolaris to pro- 
duce aggravation of existing gastric trouble reaches its maximum 
in cases where there is retention of food residues. This happens 
when the muscular walls of the stomach are in a state of atony 
and also when there is some pyloric obstruction which prevents 
the organ emptying itself. In both these conditions stomach 
dilatation is eventually produced, with the result that the stomach 
is never completely emptied. -The first condition is a very fre- 
quent concomitant of neurasthenia and allied states. It is easy 
to see how pyorrhoea can at once be predisposed to by neuras- 
thenic states and at the same time increase the neurasthenia by 
causing gastric trouble through its interference with gastrointes- 
tinal digestion under the conditions mentioned. 

Herschell 2 is of opinion that many of the chronic indigestions 
are due to continual absorption of pus into the system from a 
pyorrhoea alveolaris. In these cases he remarks there should be 
other evidences of the absorption of toxins, such as pigment spots, 
urticaria, etc. Fitzgerald points out that the bacterium coli com- 
mune is a constant inhabitant of the oral cavity, and, as a rule, 
seemingly harmless. Under the influences of a culture medium 
such as would be furnished by a pyorrhoea or an inflammatory 
state of the gum, this bacterium might, as elsewhere in the 
mucous membrane, acquire sufficient virulence to produce serious 
disturbances of the system, such as colitis, dysentery and cholera 

Clinical Journal, March (i, 1899. - Indigestion, 189."). 





There are many instances in which interstitial gingivitis takes 
place, with absorption of the alveolar process and exfoliation of 
the teeth, without calcic deposits. In such cases the blood is 
charged with only sufficient lime salts for the nourishment of the 
body. The waste products are carried off with the excreta. In 
absorption of the alveolar ju-ocess, inflammation does not seem to 
extend to the capillaries, the result of which is, this waste mate- 
rial is curried into the circulation. In this way, calcic material 

Fig. CS. 

does not collect in the fluids and upon the teeth. In those cases 
in which pus is not present (there being a lessened amount of 
carbonic acid) calcic deposits rarely take place. The percentage 
of teeth so found, however, is not so large as those with deposits. 
Examination, by a magnifying glass, of a recently extracted 
tooth (whose root is covered with serumal deposits) shows the 
lime deposited in a manner resembling that of stalactite forma- 
tion. The deposits often stand out distinctly independent of each 
other ( Fig. 68). This condition is due to deposits from the blood, 
resultant on biochemic changes in the inflamed tissues. Blood 


stasis occurs in the gum tissue, fibrous tissue of the periosteum, 
peridental membrane and alveolar process, through which last 
much of the blood circulates. This stasis may be consequenl 
upon conditions varying from simple inflammation to disease of 
the endothelium, producing endarteritis obliterans. 

The blood has become surcharged in all constitutional dis- 
eases, but more especially in kidney lesions. Deposits occur in 
the fluids and upon the roots of the teeth. Frequently the 
deposit is found only on one side or only at one particular spot 
on the side of the root ; again at the apex, when the pulp is 
destroyed. It may encircle the root. The inflammatory process 
may therefore be circumscribed as to area or the whole tissue 
may be involved. The deposit is circumscribed in the area of 
inflammation. The calcareous matter absorbed from the alveolar 
process in the immediate vicinity of the root is not improbably 
soon deposited upon the root or roots because of the impeded cir- 
culation. 1 "Ossification, as has been well remarked, is an active 
development in which the tissues are abundantly supplied with 
blood. There is a rapid cell proliferation, and the calcareous 
matter forms an intimate and permanent union with the tissues. 
Calcification, on the other hand, is passive, and indicates an 
impaired vitality. Calcification begins as a rule in the intersti- 
tial tissue. In regard to the origin of the calcareous salts, it is 
generally believed that they come more or less immediately from 
the blood, although Rokitansky supposes that they were formed 
by a metamorphosis of the tissues involved." 

Calcification is due to two varieties of causes: general and 
local. The former are dependent upon changes in the blood or 
its circulation, due, for example, to disease or senile change. In 
composition the blood may he so altered as to contain an abnormal 
amount of calcareous matter. This effect is most commonly pro- 
duced by absorption of lime salts from osseous tissues which are 
the seat of extensive caries, osseous cancer, osteosarcoma or osteo- 
malacia. The calcareous matter thus taken up is conveyed to 
other and often remote parts and there deposited, constituting the 
" metastatic calcification " of Virchow. Kiittner, of St. Peters- 
burg, has observed a rapid calcification of nearly all of the small 
arteries as a result of caries involving the dorsal and lumbar 

1 Wood's Handbook of Medical Sciences, Vol. I, page 74:!. 


vertebrae in a nineteen-year-old boy. Virchow has observed a 
case in which, as a result of bone cancer (affecting nearly all of 
the larger bones, particularly the borders of the vertebra and the 
skull), the calix and pelvis of the kidneys, the lungs, parenchyma, 
and the stomach mucous membrane were calcified. 

Circulation of the blood may be retarded and thus favor pre- 
cipitation of calcareous matter normally held in solution. To this 
is chiefly due the frequency of calcareous degeneration from 
general loss of vitality. 

Calcification rarely, if ever, depends upon general causes 
alone. There is, as a rule, a local influence. Very often this is 
due to preexisting chronic inflammation. Old accumulations of 
pus and exudates are exceedingly prone to calcification. The 
deposit frequently occurs also in fibrous walls surrounding the 
accumulation. A mere loss of function predisposes to calcification. 
Such is the case in and about the tissue of the alveolar process. 
The decalcified material from the alveolar process collects in the 
soft tissues as well as upon the roots. In his paper George T. 
Carpenter ' asks the question : Can a tissue be absorbed and still 
remain as debris in the pocket? Such is the condition found, 
and this can be easily proven. Take the contents of a pocket 
and dissolve it in hydrochloric acid, add three times its bulk of 
water, to this add ammonia, which will precipitate the phosphate 
and the calcium. The same results may be obtained by rinsing 
a freshly extracted tooth of a pyorrhoea case in cold water. 
With a stiff brush remove the accumulation and place it in a 
test tube, add hydrochloric acid and more water if necessary. 
To this add a solution of ammonia and the lime salts are precipi- 

Roots of teeth that have become entirely denuded of peri- 
dental membrane and bathed in pus accumulate large quantities 
of calcic deposits direct from the absorption of the alveolar 

Difference of opinion exists as to the nature of the process 
immediately involved in precipitation of lime salts. The simplest 
and seemingly most logical explanation is that the process is 
similar to that involved in the formation of stalactites. A certain 

1 Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhea 


amount of calcareous matter is a normal constituent of the blood. 
Herein it is held in solution by carbonic acid, always present in 
sufficient quantity for this purpose. When the circulation is 
impeded the free carbonic acid (because of its great diffusibility) 
is readily absorbed by the tissues or goes to form new compounds, 
necessitating a precipitation of the calcareous matter. Calcareous 
matter may be deposited in either a fibrous or fluid matrix. It 
shows a preference for newly formed fibrous tissue, particularly 
when this is associated with old tissue undergoing fatty degenera- 
tion and absorption. In a fibrous matrix the infiltration usually 
begins in the intercellular substance, but may involve the cellular 
elements at a later period. In a fluid matrix (like pus) the 
granules are frequently deposited primarily within the cells. The 
process may advance slowly or rapidly. When local causes exert 
the chief influence it is more limited in area of invasion than 
when there is a general factor in its production, as in the meta- 
static forms. 



The .clinical history of interstitial gingivitis is essentially that 
of any other disease of the mucous membranes. The disorder 
responds quickly to treatment at its outset. Later, its complica- 
tions and the extent of structure involved render treatment very 
inemaeious, and always insure loss of the tooth. As the general 
surgeon's duty is to save life, if need be, at the expense of limb 
or organ, but to save these last if possible, so the dental surgeon's 
duty is to remove the teeth, if need be, for the benefit of the 
general health, but to save them, when possible, for the same 
reason. The patient, therefore, should be told frankly at the 
outset of interstitial gingivitis, that it is a condition requiring 
time for its treatment, and should not be given that prognosis 
too frequently made of quick cure. To such a prognosis many 
a case of constitutional disorder is due. The dentist is a practi- 
tioner of a surgical specialty, not a mere tooth-puller. The sur- 
gical side of dentistry has received too much attention, however; 
the medical or prophylactic too little. Patients are beginning to 
pay more attention to the prophylaxis of the teeth and jaws, and 
need but little encouragement and instruction to see the absolute 
necessity of early prophylaxis and treatment of interstitial gin- 
givitis. The trend in general medicine is to prophylaxis, and 
this has undoubtedly so impressed patients as to open the way 
for dental prophylactic suggestions. Viewing the question from 
the narrowest standpoint of remuneration, the dentist could not 
fail to profit by instructions to his patients on prophylaxis. He 
certainly tails in his duty as the member of a learned profession 
by not doing this. Furthermore, with the known necessity for 
prophylaxis, it is an open question whether the failure to inform 
the patient of the clangers of the incipient disease could not be 
successfully pleaded as a basis for a malpractice suit. 

From the etiology of this disease, the treatment would appear 
simple and easy. 


Early diagnosis is not difficult, since the simple inflammation 
of the gums is easily recognized by the patient. Bleeding when 
the toothbrush or toothpick is used can never be mistaken. 
The dentist with his accomplished eye can readily detect the 
slightest change in color or puffiness around the necks of the 
teeth or of the festoons between the teeth. Redness, puffiness 
and bleeding are pathognomonic of this disease in its incip- 

Few dentists have, however, given this stage of the disease 
any thought, albeit they have filled the teeth of their patients 
from year to year. 1 have in mind three patients with loose 
teeth and inflammation extending throughout the peridental 
membrane and alveolar process, who had been under an old 
practitioner now retired from practice. The patients had never 
had the gums treated or even their teeth cleaned. This is not 
an uncommon occurrence. The excuse usually made by the 
dentist is that he cannot get paid for his time. Gingivitis is 
a disease which the dentist is as much bound to treat and cure 
as any disease of the month and teeth. It is a part of his 
specialty which should not be ignored. It is claimed that the 
dental profession is overcrowded. Were this disease treated 
until the gums were placed in a healthy condition, there would 
he practice enough for as many more dentists as there are today. 
The busy dentist of today could attend only to one-half the 
patients whom he now serves. 

The treatment, then, should be prophylactic in its nature, 
preventive rather than corrective. The disease and treatment 
is not unlike an inverted pyramid : the farther from the apex or 
beginning, the more difficult and hopeless the task becomes. 
Since the teeth have nothing directly to do with this disease, 
they should be ignored. In the early stages, the gums should 
receive proper attention. These, like other parts and organs of 
the body, must be exercised to be kept healthy. The gums 
should be properly massaged, just as the liver, kidneys or skin 
are when they are not doing proper work. This can he accom- 
plished by properly made brushes. The ordinary toothbrush is 
not adapted to the work under discussion. It will brush the 
teeth hut not reach the gums. What is needed is a massage 
hrush that will miss the teeth to a certain extent, but will reach 


the gums and contract them tight around the teeth, thus pre- 
venting the accumulation of foreign substances. The patient 
should be instructed with this single idea in view, " that the 
gum margin is to be exercised and stimulated and not the teeth, 
which must be ignored." A brush, properly made for gum 
massage (Fig. (39), will do sufficient work upon the teeth with 
the aid of the floss silk and toothpick. It should haVe printed 
upon the handle, in large letters, " gum massage brush." The 
handle should be bent a little more than the " prophylactic," so 
that the end containing the bristles can he brought in contact 
with the gum, posterior to the central incisors, upper and lower, 
and around the third molar teeth. There should be a tuft of 
bristles at the point with a space for the teeth. The tuft should 
he longer than those on the body of the brush. This tuft will 

reach the gums at all points inside of the mouth and around 
the molars. The bristles on the body must have spaces between 
them, so that when the upward and downward movement is 
given, the bristles will go between the teeth and reach the gum 
festoons. The bristles must be medium and hard. The quality 
of bristles must depend, however, upon the condition of the 
gums. If they be soft and spongy, the medium may be used. 
If the processes are heavy and thick, the gums swollen and 
engorged with blood, hard bristles must be used, Soft bristles 
(although sometimes recommended) should never be used. 

The antique theory that vigorous stimulation is injurious is 
too much accepted. Barrett, 1 for example, says, "massage of the 
gums with the ball of the finger and by the frequent use of a 
rather soft brush should be resorted to." Beodecker ' remarks 
that too frequent application of the toothbrush is sufficient to 

1 Dental Cosmos, 1883, page ">•'!:.'. 

2 Anatomy ami Pathology of the Teeth, page :;ii.">. 


produce papillary hyperplasia. Tomes 1 says, " in my own expe- 
rience I have found that frequent and vigorous rubbing of the 
gums with the finger, shampooing them in fact, has often been 
productive of great advantage, the patient of course being cau- 
tioned not to rub the actual edge; but even on this point there 
is difference of opinion, for in a recent paper on the subject, rest 
and the avoidance of all friction is advocated." Dr. Meyer L. 
Rhein 2 in introducing the "Prophylactic Toothbrush" to the 
profession, says, in his article on "Oral Hygiene," each brush 
conies inclosed in an envelope, upon which are printed directions 
for the intelligent use thereof, and the following caution : "Never 
pass the brush across the teeth, as this movement destroys the 
delicate membrane which attaches the gum to the teeth, causing 
recession of the gum, and ultimate loosening and loss of the 
teeth." Citations of this could he multiplied, showing the gen- 
eral impression is that the gums should not he stimulated to any 
great extent; that the finger, a soft cloth, or a very soft tooth- 
brush alone should he employed. The use of the finger is a 
superstition which is handed down from generation to generation 
without the slightest critical analysis. If the advocate of this 
use would try the experiment, he would see how impossible it 
would he to bring it in contact with all the tissues of the mouth 
that are involved in this disease; were it possible, the lingers, 
cloth and soft toothbrush would not accomplish the desired 

No brush should he used whose bristles are softer than the 
medium ; very often these, used once or twice and dipped into 
water or mouth washes, become so soft as to he wholly unfit for 
use. It is always a good plan to have two brushes to be used on 
alternate days. In this way one can dry while the other is being 
used. The general opinion has been that friction upon the gums 
was detrimental on account of the resultant tendency to absorp- 
tion of the gums. While this may exceptionally he true, it is 
not true of a majority. Should milk, arsenic, iron, strychnine or 
quinine he entirely abolished as remedies because occasionally a 
person presents untoward effects? If the alveolar process he 
very thin over the roots of the teeth, especially the cuspids, the 

1 Dental Surgery, page, 704. 

-New England Journal of Dentistry, October, 1884. 


patient must be instructed so to use the brush as not to over- 
stimulate these particular parts. In such cases the inner alveolar 
process and gum tissue may be stimulated with impunity and 
with the hardest brush. Again, if the chronic interstitial gingi- 
vitis be of long standing, or even if chronic gingivitis has 
been present for some time, stimulation of the brush will 
cause the gums and mucous membrane to recede until hard, 
sound, healthy structure has been secured. Then absorption 
will cease. In most cases absorption and contraction of the gum 
tissue will take place to a more or less marked degree. If 
absorption of the alveolar process has taken place and the gums 
are puffy, red and swollen, a disease exists to be cured, regardless 
of consequences. The alveolar process and gums will never 
return to their original jjosition, but it is a decided advantage to 
have a healthy mouth, even if the alveolar process and gums 
have slightly receded. 

I have used medium and stiff brushes in my practice for the 
last fifteen years and have failed to see any ill results. For the 
past four years I have made constant experiments, with the view 
of securing the proper shape and stiffness of the bristles and have 
obtained uniform results in gum treatment. 

Proper employment of the " gum massage brush " requires skill. 
Every dentist should train his patient in the method of using the 
brush. The gingival borders should not only be stimulated, but 
the bristles should be so passed in between the gum margin and 
the tooth as to remove the debris and exfoliated epithelial scales 
which have accumulated therein. These are often the cause of 
the irritation. Unless this be done the gum or epithelial tissue 
cannot perform its functions or be restored to health. Stimulat- 
ing astringents and germicidal mouth washes should be employed 
whenever the gums are massaged. The massage should be done 
three times a day. The patient should be under the care of the 
dentist at least twice or thrice a week, so that he may direct the 
treatment, If the teeth are irregular, care and patience are 
required to reach the festoons between the teeth. After the gums 
are in perfect health, the patient should visit his dentist at least 
four times a year for further instruction. If on inspection the 
gums be found diseased at any point, the dentist can direct the 
attention of the patient to the particular locality and the disease 


be eradicated. By this method and this alone can the gums be 
kept in a healthy condition. Each patient must be given specific 
directions as to the treatment of his or her case. 

If the gums have become swollen and engorged with blood 
a different method must be employed. Here the absolute law of 
medicine obtains — "remove the cause," no matter whether of 
local or constitutional origin. If due to improper articulation 
this must he corrected. If constitutional, and due to any of the 
mineral poisons or scurvy, the system should be flooded with large 
quantities of pure water. There is uothing better to rid the sys- 
tem of poisons and impurities than flushing the blood with from 
three to five quarts of pure water a day. Cathartics should be 
employed. A Turkish hath should he used to open the ports of 
the skin, at which time the masseur should be instructed to stim- 
ulate the liver, kidneys, skin and peripheral nerves. If the 
patient suffer from disease like syphilis, tuberculosis, diabetes, 
Bright's disease, colds, including catarrh, nervous prostration, 
amemia, etc., special treatment is indicated. Remove all deposits 
and other irritants from around the teeth. 

Two decades ago, I advocated the use of the following set of 
scalers; nothing better has been produced since. They consist 
of handles, shanks bent at different angles, and blades three- 
cornered, so that they can be used in three directions without 
removing the fingers from the tooth (Fig-. 70). These are all 
delicately made, and tempered very hard. Sharp edges are 
there retained. They will reach every point where tartar can 
collect. After the deposits have been fairly well removed, the 
gums may be syringed with hot water (Cravens) to remove all 
debris. The gums should be saturated with tincture of iodin 
( C S. I'. ) or iodin and aconite, in the following manner : Have a 
number of wooden toothpicks ( Portuguese preferable) wound with 
cotton, and kept in a little box. Saturate the cotton and paint 
the gum as far as it will go. Throw this into the waste basket 
and take another, and so on until the gums are well saturated. 
From three to five picks will be required. The assistant can 
keep these in order between patients. In such cases a different 
massage Brush is to be used. One is here required that will so 
lacerate and stimulate the gums as to relieve the congestions-. 
This brush, made of coarser and stiffer bristles, should be used like 



the other. After two or three days the gums will contract, and 
healthy circulation follow. Pain will now be experienced in the 
gums. The massage must still be kept up. An astringent, 
stimulating and general mouth wash, should be used in connec- 
tion with the massage. The patient should return every other 
day for further treatment with the iodin, or iodin and aconite 
used as before. To reach an inflammation, chronic and deep- 
seated, extending into the peridental membrane, periosteum and 
alveolar process, there is nothing in medicine better than iodin, 
or iodin and aconite. This, and this alone, will reach the deeper 
inflammation. After a few treatments and constant use of the 
massage brush, the gums will contract, and other deposits which 

were overlooked at the first sitting will now be presented to 
view. If the gums be very painful at the first sitting, no effort 
should be made to remove the deposits until the inflammation 
has, in a. measure, subsided. The iodin treatment and massage 
should be conducted as suggested until the gums have been 
reduced and the pain ceases. After they have been restored to 
health, constant massage with the medium brush must be 
employed two or three times a day. The patient should return 
to the dentist as often as necessary (every month or two) to 
have the gums examined, and for further direction. 


As lias been already shown, chronic interstitial gingivitis may 
extend only to the peridental membrane, to the periosteum, or it 
may extend throughout the alveolar process with the absorption 
of the hone the entire length of the root of the tooth. Pus 
infection and serumal deposit may or may not take place. In 
the early stages of this progressive inflammation, the first is prob- 
able. If pus and deposits are present they can be treated with 
signal success according to the symptoms and as hereinafter 
explained. As already suggested, the gum massage brush must 
he vigorously used to relieve the engorged tissues of blood. 
Since absorption of the alveolar process depends upon irritation 
and inflammation, this must be removed as quickly as possible. 

In the treatment of deep-seated interstitial inflammation, 
iodin or iodin and aconite has always been regarded by physi- 
cians and surgeons as the best remedy. The gums should be 
thoroughly saturated twice or thrice weekly, as already suggested. 
If the alveolai' process be so absorbed that the tooth has become 
loose, the ease is hopeless. In such unstable tissues, especially 
when inflammation extends through the process and lacunar, 
perforating canal absorption and halisteresis is going on, reversal 
of the order so as to set the osteoblasts to tissue-building is 
hardly to be expected. The tendency is to destroy and not 
restore the alveolar process. In such cases the tooth must be 
fastened to the other teeth perfectly tight to prevent motion in 
any direction. The movement of the tooth in mastication inten- 
sifies the irritation, which in time only increases the absorption. 
Liberal use of iodin or iodin and aconite and the gum massage 
brush is all that can be done to reduce the inflammation and 
absorption as much as possible. The exfoliation is only a matter 
of time. If the tooth or teeth cannot be retained perfectly tight. 
no matter how healthy the surrounding tissues may be restored, 
the irritation produced by the loose teeth will soon set up inflam- 
mation in the surrounding tissues. The sooner the loose teeth 
are removed the better. In no case can the bone tissue be 
restored, if the matrix or cartilage be destroyed, since in this the 
osteoblasts are located. If the matrix or cartilage be destroyed, 
a fibrous union (such as occurs in the case of implanted teeth and 
the imbedding of foreign bodies in the tissues of the body) only 
is possible. 


If inflammation have extended into the periosteum, peri- 
dental membrane and alveolar process, serumal calculi are fre- 
quently deposited upon the roots of the teeth. When this has 
taken place, the calculus must be removed. This should be 
done with the utmost care, in order that adjacent tissues may not 
be injured, or inflamed parts infected with pus germs. Since 
dead bone is not present, the operator should confine his instru- 
mentation entirely to the root or roots of the teeth, with as little 
injury as possible to the adjacent tissues. The alveolar process 
must under no consideration be touched. Riggs believed that 
the edge of the alveolar process was always in a state of dis- 
integration, and that it should be so scraped as to get a fresh 
surface, on the principle of caries of bone. Many dentists are 
operating in this manner at the present time. I have elsewhere 
shown simple absorption and not caries is present. Such treat- 

ment is wholly unnecessary and contraindicated. The object of 
the removal is to allow the fibrous tissue of the peridental mem- 
brane ( after health is restored ) to tighten about the root, which 
cannot be accomplished when foreign substances are present. 
Pushing instruments must never he used, but only such instru- 
ments as have smooth and round backs, tempered very hard so as 
to retain sharp edges. These instruments should be small, with 
small points to reach depressions, and to be as universal as pos- 
sible. Such an instrument is to be found in the spoon excavator 
(Fig. 71). The shank can be bent to suit the operator. This is 
to be carried gently along the length of the root and passed 
over the deposit with a firm hand, resting the finger upon some 
other teeth. The drawing motion is invariably to be from the 
membrane, and toward the crown. The deposits are sealed off 


painlessly. The round blade being larger than the shank, and 
cutting- upon three edges, half of the root in both directions can 
be circled without removing the instrument. A similar instru- 
ment bent at the shank in the opposite direction may be used on 
the other side. After all of the roots of the teeth have been 
scaled, the spaces are to be syringed out with warm or hot 
water (Cravens). The gums are to be thoroughly saturated 
inside and out with iodin. The gum massage brush is to be used 
thrice daily as before. The patient should return twice or thrice 
a week for further instructions. The contracting gums will 
assist greatly in revealing the deposit. If deposits still remain 
on the roots (the appearance of the gums will indicate its pres- 
ence) further use of the scalers is indicated. The delicate instru- 
ments and the accustomed sense of touch will reveal the hidden 

With the precautions already noted, local anaesthesia is 
unnecessary. The smooth, round surface of the back of the 
instrument, if carefully inserted, will not produce pain. 

If the gum be painful to the touch, or if the patient be 
nervous and sensitive, application of tincture iodin may be used, 
together with massage, for a few days before scaling is resorted 
to. The sensitiveness will soon disappear, when the instrument 
may lie inserted without difficulty. 

A few years hence, the profession will regard a dentist whose 
patients have pus oozing from the gums as a prehistoric relic and 
the patient as an individual whose filth provokes the contempt of 
his fellows. In this day of antisepsis, the dentist is as account- 
able for pus infection of his patients as the physician or surgeon. 

There is no more excuse for the dentist's patient being in- 
fected than the surgeon's. If ordinary antiseptic precautions are 
taken, pus infection will not often occur. Prevent inflammation 
of the gum margin and pus infection cannot follow, no matter 
how many germs be in the mouth. This is an absolute law of 
general pathology. It has been proven by the experiments made 
by Miller, G. T. Carpenter and myself on dogs, rabbits and man. 

The illustrations of the progress of interstitial gingivitis teach 
that only the mildest treatment is indicated. Harsh treatment 
on the infiamed bone or fibrous tissue, either with instruments or 
drugs, must not be employed. Heroic treatment, such as the 


indiscriminate application of sulphuric and lactic acid and sim- 
ilar drugs in nearly or quite full strength, is not justified by the 
surgical principles of today. No surgeon would think of making- 
such an application to inflamed bone in other parts of the body 
without he wished necrosis with a desired sequestrum. Much 
less would the intelligent operator use such treatment in a transi- 
tory structure which predisposed to destruction. In a number of 
instances exfoliation of the anterior plate of the alveolar process 
has resulted from this treatment, to say nothing of the intense 
pain produced. J. M. Whitney 1 has had four cases in his prac- 
tice in which serious results followed. The first indication is to 
remove the cause. Instrumentation should be resorted to only 
to remove tartar and calcic deposits. This must be done in such 
a manner as not to infect the deeper inflamed tissue or carry the 
products of inflammation into healthy tissue. The treatment of 
infected tissue within and about the alveoli is not unlike treatment 
of abscesses and ulceration elsewhere. Such drugs as are used 
in abscesses and ulcers in other tissues are indicated here in the 
same strength. If strong drugs be used they should not be per- 
mitted to remain in the tissue, lest necrosis of the alveolar process 
occur. They must be diluted or removed altogether after they 
have accomplished their purpose. Very serious results have 
occurred from careless use of drugs. When abscesses have 
formed they should be opened and hydrogen peroxid — or, which 
has answered my purpose equally well, hot water (Cravens) — is all 
that is necessary. More difficult is treatment of ulceration of the 
tissue near the root of the tooth. Ordinary cases will heal after 
hot water or hydrogen peroxid have been applied. In some 
cases the pus germs have followed the inflammation along the 
course of the vessels quite a distance into the interstitial tissue. 
In such cases they are difficult to reach. A small syringe 
(George T. Carpenter's) may be employed, or the drug may be 
carried to the part on the end of a long, thin orange-wood stick. 
In all cases the drug must be directly applied to the part in order 
to have beneficial results. Applications of iodin should be used, 
as already suggested. Iodin carried to the ulcerated surface often 
suffices to destroy the pus secretion. Ordinarily one or two 
applications is sufficient. Occasionally calcic deposits are located 

1 International Dental Journal, April, 1899. 


in front of the infected surface and the drug does not reach the 
part. In such eases the deposit must be removed. If the pus do 
not cease at the first, second or even third application, this is not 
because the drug is not sufficiently strong, Imt because it does not 
reach the infected part. Continued applications of iodin exter- 
nally and internally, carried well up between the roots of the 
tooth and the alveolar process will, in time, produce the desired 
result. When pus ceases to flow, antiseptic treatment must stop. 
The iodin and massage treatment must then he pushed until the 
interstitial inflammation has been reduced and the gums con- 
tracted tightly about the necks of the teeth. 

After the tissues have been placed in a healthy condition, 
they will require the constant attention of the operator, since, 
like other tissues of the body when once diseased, favorable con- 
ditions will cause a recurrence. The patient must return to the 
operator frequently so that he can advise as to the use of massage. 

I have elsewhere shown that uric acid ( like lactic and other 
acids, mercury, lead and brass poisoning) may produce local 
irritation in a small number of cases, resulting in interstitial 
gingivitis. Uric acid is absorbed into the blood and is thus car- 
ried to all parts of the body. As mercury, lead, brass and potas- 
sium iodide collect in the tissues of the alveolar process, on 
account of the sln<;'o'ish blood supply, so does uric acid, setting 
up inflammation. These cases are easily diagnosed, since, unlike 
the ninety-four per cent of cases that begin at the gum margin 
without pain and are of long standing, these set up a spontaneous 
inflammation in an otherwise healthy alveolar process. This 
may occur about one tooth, or more may be involved; usually it 
involves the tooth or teeth standing alone or having improper or 
no articulation. The inflammation is followed by acute pain. 
If this be not reduced an abscess may, as elsewhere shown, form 
at some locality about the alveolar process. Inflammation will 
extend throughout the alveolar process and rapid absorption 
result. The tooth will loosen in the socket. If systemic treat- 
ment he not at once instituted, exfoliation of the tooth or teeth 
shortly ensues. The first thing indicated in such cases is an 
application of iodin to reduce inflammation and pain. The urine 
for twenty-four hours should be secured for chemical analysis. 

The materials and appliances necessary for the purpose of 


making an examination of the urine for uric acid are many and 
the method requires considerable time. The dentist can do the 
work, but it will be much more satisfactory (if he must know the 
quantity eliminated each day) to send it to a competent chemist. 
Should he desire to make the urine analysis, I should recom- 
mend the method suggested by Bartley * in which he says, " The 
estimation of uric acid is usually attended with much difficulty 
and consumption of time. The author has devised the following 
volumetric method, which is fairly rapid, reasonably accurate 
and requires little skill. It can therefore claim a place as a 
clinical method. The process is based upon the well-known 
fact that uric acid is completely precipitated from its solutions 
containing an excess of ammonium-magnesium mixture and 
ammonium hydroxide, by silver nitrate. When the precipita- 
tion is complete, the slightest trace of silver in solution is shown 
by the dark color j>roduced in a drop of the clear solution by a 
soluble sulphide." The method of procedure is thus explained, 
should the uric acid excreted in twenty-four hours be less than .8 
grams or 10.8 grains it is safe to say that it is retained in the 

Imperfect tissue metabolism, as V. A. Gudex, 2 of Milwaukee, 
has shown, results in the formation of the following acids and 
substances: uric, hippuric, oxaluric, carbonic, lactic and lac- 
tates, caprylic, caproic, valerianic, butyric, propionic, acetic, 
stearic, oleic, palmitic, formic, eholalic,. tuarilic, damaluric, 
damalic, and succimic acids. Of these, the uric acid seems to act 
least as an irritant. The urine, therefore, should be examined 
for general acidity, the general treatment of which will accom- 
plish all that is to be desired. A safe and delicate test can be 
accomplished by determining the alkalinity of the urine, saliva, 
perspiration, expectoration and dejection. The dentist is fortu- 
nate in this because he has every convenience at hand. Lieb- 
reich's methods of the use of plaster of paris plates as elaborated 
by A. H. Hoy, 3 of Chicago, is most admirably adapted for this 
purpose, since the test can be readily applied. To make the 
plates, mix a very thin quantity of dental plaster to the con- 

1 Medical Chemistry, page 641 ; fifth edition. 

2 Items of Interest, May, 1891). 

3 Eating and Drinking. 


sistency of cream, care being taken to thoroughly incorporate 
the plaster. Take two panes of window glass, cut four pieces of 
wood three-sixteenths of an inch in thickness and place one at 
each corner of the glass; now pour the plaster into the center, 
place the other plate of glass above and press it down upon the 
blocks of wood. By this method a very smooth surface can be 
obtained. Make a round cutter out of tin, the size of a twenty- 
five cent piece. Remove the upper piece by sliding it off, cut 
out round disks just before the plaster hardens. These are pre- 
pared in the following manner: A solution of litmus in 12 
parts of water is rendered. alkaline or bright blue by adding a 
few drops of aqua ammonia. After the disks have become per- 
fectly hard, the smooth polished surface is to be painted with 
the solution, using a camel's-hair brush. Two or three applica- 
tions are to be made, until an even blue stain is obtained. Have 
a solution of chemically pure sulphuric acid, two parts in five 
hundred of distilled water, ready in a bottle, and a bottle of dis- 
tilled water. To prepare the disk for the test, scrape one-half 
of the dark blue surface of the plate until a slight blue sur- 
face is obtained. This requires the removal of only a slight 
amount, since the blue stain only penetrates a short dis- 
tance. With a small brush, dipped into the acid, draw it quickly 
over the surface exposed, giving a red appearance to the field 
adjoining the blue. 1 A bit of cotton, wound around the end 
of a toothpick wet with distilled water and applied to the 
two colors, will produce no change, thus proving everything to 
be in working order. The fluid to be tested — urine, saliva or 
perspiration — may now lie applied. When possible, the exudate 
must be applied to the test as soon as it leaves the body, care 
being taken to apply a fixed amount each time. Apply the 
fluid to be examined to both the blue and red fields. When 
saliva is used, the mouth must be rinsed two or three times and 
the quantity first sucked out of the ducts must not be used. 
Fresh saliva direct from the glands should only be used. The 
plates, alter they have been used, may be re-stained and used 
indefinitely. The dentist should make repeated tests of the 
secretions of healthy individuals under different conditions 

1 It is almost impossible to obtain a satisfactory permanent red litmus. By this 
method the red and blue fields stand out in bold contrast. 


before studying those of diseased conditions. This method is 
a more delicate test than it is possible to make even with 
litmus paper. Litmus paper often fails to reveal reaction, 
which will be most obvious by this method. 

The secretions of the body, if found to be acid, must be 
placed in an amphoteric condition as soon as possible. An 
amphoteric condition is a reaction of the urine, by which 
both the blue and the red litmus are affected. If the red 
becomes blue and the blue red it indicates that there is an 
amphoteric reaction. The salt giving the alkaline reaction is 
the trisodic phosphate ; that giving the acid reaction is the mon- 
asodic phosphate. When a uniform color is produced it shows 
that the alkaline and acid salts are being properly excreted in 
proper amounts with no excess of free acid. 

The normal urine specific gravity is 1018 to 1025. To 
determine the specific gravity, the morning urine should be used. 
If about 1018 or lower and acid, it is due to fermentation in 
small intestines. In such cases avoid yeast bread, acid fruits, 
wines, vinegar and all acids. If specific gravity is 1025 or 
more and acid, avoid meats. From five to seven pints of pure 
water should be taken each day, to flush the blood and kidneys 
and thus cleanse the system. Certain patients, especially neu- 
rasthenics, nervous dyspeptics and many lithsemics, have a 
repulsion to pure water. The water can be adjusted to these 
idiosyncrasies by the employment of lithia or other effervescent 
tablets. The main object is to preserve in such cases the promi- 
nent idea of the water being medicated. Local treatment, as 
elsewhere described, should here be resorted to. Besides the use 
of water, dietetics in dentistry involve chiefly a conservative 

Under most conditions of suboxidation and imperfect elimi- 
nation, as elsewhere shown, the gums are forced to assume an 
excretory energy to which they are unequal. As a consequence 
a foundation is laid for interstitial gingivitis, which, in all of its 
types, may seriously threaten the integrity of the teeth. Nay, 
more, by furnishing a culture medium for pus microbes it may 
threaten the general health, not only through systemic infec- 
tion, but also through its interference with proper gastro-intestinal 
digestion. Among the restrictions in diet which dental hygiene 


demands is, first, a restriction in foods and water containing an 

excess of lime salts, which produce tartar. As excess of foods 
containing nitrogen, when aided by an imperfect assimilation of 
the carbohydrates, tend to produce constitutional conditions like 
lithaemia, gout, etc.. which affect tissue nutrition of the gums, these 
foods require restriction and adaptation to the particular case. 
While the constitutional condition underlying lithaemia markedly 
predisposes to gum irritations and inflammations, its value as an 
exciting cause is hut slight. Lactic acid, as has been elsewhere 
pointed out, is a more marked local excitant. In the constitutional 
production of lactic acid, ingestion of the carbohydrates without 
assimilation plays a part. Scurvy, which may seriously threaten 
the integrity of the gums, requires the usual dietetic treatment. 
While there are indications of the untoward effects of infantile 
scurvy on the gums, the pathology and consequences of it are 
not as well known as those of scurvy in the adult. The 
researches on scurvy in the infant tend to show that it results 
from a monotony of diet rather than the absence of any article of 
diet. The dietetics of dentistry, therefore, involve precisely the 
same principles as do the treatment of the constitutional con- 
ditions which are the predisposing factors of the gum disorders. 
During the entire process of treatment (indeed before the 
treatment begins) a suitable mouth wash should he used two or 
three times a day. This should be composed of a germicide, 
antiseptic disinfectant and deodorant, and should he used at the 
time of the massage. 



Alexander, H. C. B 145 

Allbright 3 

Andrews, R. R 89 

Arcovy 4 

Barlow, Thomas 95 

Barrett 174 

Bartley 184 

Black . 5, 34, 41, 47, 48, 51, 53, 5G, 98 

Beodecker 174 

Bondurant 91 

Bon will 2, 157 

Brown 2 

Brubaker, A. B 08 

Buzzard 97 

Calve, Marshall de 2 

Carpenter, G. T. 125, 165, L70, 

181, 182 

Cartright, Hamilton 4 

Clowes 3 

Coles, Oakley 4 

Collins, J 66 

Congdon 68 

Cravens 181, 182 

Cruveilier, C 92 

Dana, C. L 97 

Dickinson, Howship 78 

Ebner, Von .... 56, 153, 158, 160 

Eisenhart 159 

Enderlin 76 

Essig, C. J 3 

Evans, W. A 123 

Farrar, F. N 4 

Fitzgerald 9, 68, 167 

Flower, Alsop 14 

Foster 11 

Fuchard, H. A 2 

Galippe . . 4,12,122,123,124,151 

Geddings, H. D 75 

Gray 37 

Gudex, V. A 184 

Hektoen, L 127, 155 

Hertwig, 56, 146 

Herzog, M 124 


Hirt 97 

Hogben 94 

Howell 77 

Hoy, A. H. ........ 184 

Ingersol, L. C 4 

Izklai, Joseph 4 

Jacobi 95 

Jacobson . . 75 

Joirac 2 

Jourdain 2 

Kaecker 2 

Kaufinann . . .61, 154, 157, 158 

Kirk 12, 68 

Koch 12, 151 

Kolliker .... 30,33,56,62, 161 

Kuttner 169 

Magitot . . - 2, 7, 53, 55, 57, 58, 91 

Mailhol 11 

Malasses 4 

Malenfont 79 

Miller. . 8,82,89,122,123,125,181 

Mills 3 

Minot 42, 53, 56, 146 

Morgan, de 31 

Niles, N. S 3 

Noyes, Frederick 48 

Patterson 4, 6, 8, 89 

Pedley 6, 7 

Pierce, C. N. . . . 8, 12, 37, 68, 96 

Quain 10, 11 

Raw Is, A. 4, 95 

Rechlinghausen, Von 159 

Reese 4 

Reeves 68 

Rehwinkle 3 

Rhein 68, 175 

Riggs, J.T 2, 180 

Robin 53, 55, 57, 58, 91 

Rokitansky 169 

Rose 54 

Salisbury, J. H. . . . 69,71, 7'.' 

Sayre, Charles E 14 

Schefi 2 




Scheheoetskey 78 

Schmidt, C 73, 74, 70, 78 

Serres 47 

Sirletti 3 

Starr, A. R 5 

Stevenson 78 

Sudduth, W. X. ... 5, 6, 7, 8, 161 

Sutton, Bland 7 

Talbot, E. S 5, 47 

Tomes . . 
Virchow . 
Walker . . 

Wesener, J. A 09, 70 

Whitney, J. M 182 

Zawadsky 76 

Ziegler 28, 158 


. . 27, 31, 175 

31, 62, 63, 153, 160 

. . . 169, 170 





Acadians, Teeth of 1 

Alveolar Process 21 

Absorption of 147 

Absorption 157 

Absorption and Trophic 

Change 162 

Changes 149 

Dermal Bones 96 

Germ Infection . . . . 96 

Hypei'trophy of 29 

Antimony 144 

Arsenic 144 

Bone Absorption 59 

Bone Building 59 

Brass 144 

Interstitial Gingivitis ... 94 

Bromides 145 

Calcic Deposits _ 168 

Calcospheritea 41, 133 

Calculi, Salivary 78 

Carnivora, Interstitial Gingivitis in . 14 
Catarrhal Idiosyncrasy .... 5 
Cave Dwellers, Teeth of ... . 1 

Cementoblasts 42 

Cementoclasts 61 

Children, Degenerate 89 

Diathetic 89 

Interstitial Gingivitis in . . 81 

Neurotic 89 

Pyorrhoea in 89 

Debris, Epithelial 55 

Dental Operations and Alveolar Pro- 
cess 150 

and Bone Absorption . .150 

Dental Shelf 55, 56 

Degeneracy and Degenerate Tissues . S7 

Dentitions, The Three 84 

Dogs, Interstitial Gingivitis in . 14, 98 
Mercuric Interstitial Gingi- 
vitis in 117 

Pyorrhoea Alveolaris in . . 98 
Ebner, Von, Vessels of .... 31 
Egyptians, Teeth of 1 


Embryology of the Tooth .... 46 
Endarteritis Obliterans .... 154 
and Tuberculosis .... 155 
Exanthemata and Catarrhal Gingi- 
vitis 7 

Follicle, The Dental 55 

Gingivitis 5 

Expulsive 11 

Interstitial 9 

and Pyorrhoea 9 

Glands of Mucous and Peridental 

Membranes 47 

Greeks, Teeth of 1 

Gums 42 

Halisteresis . . . . 61, 62, 153, 158 

Haversian Canals 30 

Heredity 13 

Interstitial Gingivitis . . . . 10, 12 

Antimony 144 

Arsenic 144 

Atavism and 83 

Auto-Intoxication and ... 66 

Bacteriology of 122 

Brass 144 

Bromide 145 

Carnivora in 14 

Causes 12 

Degeneracy and 86 

Dogs 98 

Environment and .... 84 

Heredity and 83 

Heredity in 13 

Inorganic Salts and . 73 

Iodide 145 

Lactic Acid and 152 

Mercuric 142 

In Dogs 117 

Nerve Phases of .... 13 

Pathogeny of 151 

Plumbic 143 

Pyorrhoea Alveolaris and . . 162 
Scorbutic in Man . . . .127 
Scurvy and . . . 13, 65, 94 




Interstitial Gingivitis — 

Tartar and 148 

Theories of 65 

Toxic Causes of . . . .13, 92 

Treatment ....... 172 

Tropho-Neuroses and . . 66, 92 

Uric Acid and 68 

Iodides 145 

Jaw, Evolution of 149 

Evolutionary Changes in . . 20 
Racial Changes in .... 20 
Lake Dwellers, Teeth of ... . 1 
Lactic Acid and Interstitial Gingi- 
vitis 152 

Lacunar Absorption .... 62, 153 

Lead 143 

Interstitial Gingivitis and . . 94 
Locomotor Ataxia and Gum Dis- 
order 13 

Mercury 142 

Interstitial Gingivitis and . 93 
Mouth Breathing and Catarrhal Gin- 
givitis 7 

Mucous Membrane, Glands of 47 

Histology of 42 

Mucus, Bactericidal Function of . . 88 

Odontoblasts 42 

Osteoblasts 42 

Osteoclasts 61 

Osteomalacia .... 62, 146, 159 
Papillary Layer, Comparative Anat- 
omy 47 

Paretic Dementia and Gum Dis- 
order 13 

Perforating Canal Absorption . 62, 153 
Pericementitis Phagadenica ... 5 

Peridental Membrane 33 

< Hands of 47 

Inflammation 1 

Periosteum 33 

Periostitis Alveo-Dentalis ... 2 

Dentalis 2 

Pockets and Interstitial Gingivitis . 152 


Potassium Iodid and Interstitial 

Gingivitis 94 

Pregnancy and Osteomalacia . . . 159 

Primitive Races, Teeth of ... 1 

Pyorrhcea Alveolaris, Bacteriology of 162 

Catarrhal Idiosyncrasy . . 5 

Causes of 2 

Constitutional Causes . 3, 4, 5 
Constitutional Effects of . . 167 

Degeneracy and 5 

Dogs 98 

Eruptive Fevers .... 7 

History 2 

Intestinal Disorders from . . 167 

Lactic Acid 8 

Nervous Causes 3 

Parasites and 8 

Pathology of 6, 7 

Syphilis and 8 

Systemic Disease and ... 8 

Uric Acid and 8 

Scurvy 96, 127 

Sodium Chloride and Interstitial 

Gingivitis 95 

Stomatitis Catarrhalis 6 

Teeth, Changes in 146 

Changes in Position of . . .28 

Decay of 147 

Embryology of 146 

Irregularities of 148 

Periods of Evolution . . . 146 
Periods of Involution . . . 146 
Trophic Disorders of ... 96 

Third Molar 149 

Disappearance of .... 21 

Tooth Embryology 42, 53 

Form Changes 149 

Transitory Structures . . . .20, 147 

Tropho-Neuroses 13, 96 

Ulitis 11 

Uric Acid and Pyorrhoea Alveolaris 3, 8 
Volkmann's Canals 31 

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